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Mud-to-Mozart Atheology (Or, Who are the real skeptics?)

I find the “skeptic” claim on the part of Darwinian materialists very interesting and equally illuminating. Darwinists exhibit no skepticism whatsoever about the thesis that physical stuff turned into Mozart by chance. (Don’t try to deny this, Darwinists, that is the essence of your claim. You can try to obfuscate with legion “peer-reviewed scientific papers,” but you’re not going to fool me and many others about what you are actually promoting and advocating.)

I choose Mozart not just because I am a classical concert pianist, but because his existence epitomizes everything that Darwinian theory is totally powerless to explain.

Darwinists, claiming to be skeptics, actually exhibit the antithesis of skepticism — making transparently ludicrous claims and providing a never-ending stream of unsupported extrapolations, based only on wildly imaginative speculation with no empirical support.

How is it that Darwinian atheists are the only ones who get to declare themselves legitimate skeptics? Is mud-to-Mozart-by-chance philosophy the only worldview immune to skeptical inquiry?

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397 Responses to Mud-to-Mozart Atheology (Or, Who are the real skeptics?)

  1. This stuff isn’t any better than Ken Ham’s line he tells to school children, which is that evolution is “goo to you via the zoo”. Gimme a break.

    1. Evolution isn’t a chance process. Natural selection is an anti-chance, nonrandom process. That’s why it’s called “selection”.

    2. Evolution is about the evolution of populations and species. The special features of individuals, particularly rare individuals like Mozart, require additional explanation.

    3. Evolution gets you to stone-age humans. Most of what is interesting after that is not evolution, it’s culture. There was rather a lot of cultural development before you got Mozart. Pretending that “evolution” is supposed to explain stuff like that is just silly. You might as well be annoyed with chemistry for not explaining Mozart.

    4. We know evolution happened because we have the fossils which show it happening. The skeletal features of Mozart (and everyone else) have emerged very gradually over millions of years. Click the link, if you’re brave enough:

    http://www.talkorigins.org/faq.....inids.html

    You need to explain these fossil data, not just toss around ignorant invective.

    Points #1-4 are well-known to anyone who knows a little science, and ignoring them means that you won’t be taken seriously by scientists, and you won’t deserve to be. Just another creationists with uninformed emotional objections, rather than real ones.

  2. Is mud-to-Mozart-by-chance philosophy the only worldview immune to skeptical inquiry?

    I find it equally incredible to believe that an unidentifed designer simply poofed everything into existence. So where does that leave us?

  3. Perfect!

  4. 4
    material.infantacy

    It leaves us with absolutely nothing poofing absolutely everything into existence. So here does that leave us?

  5. The skulls from a-n are obviously similar. From Pan troglodytes through homo. The changes in the skulls are less interesting than what was changing inside the skull. The differences in skull variations from a-n are minimal compared to vast differences in the brain represented by skull a, and the brain represented by skull n. It looks like a reasonable account of common ancestory with respect to the skulls, but the changes to the brain are not thoroughly explained simply by mut+sel.

  6. You have to look at the entire background of an argument. Take unaided materialistic explanations back logically to where they could begin and you get what material.infantacy has explained above.

    With materialism you have nothing creating everything. With theism you have the necessary first cause already eternally existing, from which everything else comes into existence. Makes a whole lot more sense, such that even some non-theists view it as reasonable. Even Dr. Liddle couldn’t get passed the logic of the argument several months back.

  7. With materialism you have nothing creating everything. With theism you have the necessary first cause already eternally existing, from which everything else comes into existence.

    with ‘materialism’ you can also have a first cause already eternally existing from which everything else comes into existence.

    There is no rule that says that a universe that was not willfully created has to come from nothing or have a specific start point.

  8. Not without the absurdity of an infinite regress of causes.

  9. Well contrary to Mr. Matzke’s very non-skeptical claim that lining selected (best candidate) fossils up in a (preconceived) row allows us to ‘know evolution happened’, there are prominent researchers, who certainly know the fossil record much better than Mr. Matzke does, who ‘know’ that this ‘neat little progression’ is anything but the ‘neat little progression’ Mr. Matzke has portrayed it, ‘non-skeptically’, to be.

    These following quotes, from leading experts in the field, sum up nicely what we can make of the poverty of the fossil record for ‘human evolution’:

    When we consider the remote past, before the origin of the actual species Homo sapiens, we are faced with a fragmentary and disconnected fossil record. Despite the excited and optimistic claims that have been made by some paleontologists, no fossil hominid species can be established as our direct ancestor.
    Richard Lewontin – Harvard Zoologist
    http://www.discovery.org/a/9961

    Evolution of the Genus Homo – Annual Review of Earth and Planetary Sciences – Tattersall, Schwartz, May 2009
    Excerpt: “Definition of the genus Homo is almost as fraught as the definition of Homo sapiens. We look at the evidence for “early Homo,” finding little morphological basis for extending our genus to any of the 2.5–1.6-myr-old fossil forms assigned to “early Homo” or Homo habilis/rudolfensis.”
    http://arjournals.annualreview.....208.100202

    Man is indeed as unique, as different from all other animals, as had been traditionally claimed by theologians and philosophers. Evolutionist Ernst Mayr
    http://www.y-origins.com/index.php?p=home_more4

    “Something extraordinary, if totally fortuitous, happened with the birth of our species….Homo sapiens is as distinctive an entity as exists on the face of the Earth, and should be dignified as such instead of being adulterated with every reasonably large-brained hominid fossil that happened to come along.”
    Anthropologist Ian Tattersall – curator at the American Museum of Natural History

    further notes:

    The following sources show unequivocally that ‘Lucy’, the supposed superstar of human evolution, was an ape:

    “these australopith specimens (Lucy) can be accommodated with the range of intraspecific variation of African apes” – Nature 443 (9/2006), p.296

    “The australopithecines (Lucy) known over the last several decades from Olduvai and Sterkfontein, Kromdraai and Makapansgat, are now irrevocably removed from a place in a group any closer to humans than to African apes and certainly from any place in a direct human lineage.”
    Charles Oxnard, former professor of anatomy at the University of Southern California Medical School, who subjected australopithecine fossils to extensive computer analysis;

    Israeli Researchers: ‘Lucy’ is not direct ancestor of humans”; Apr 16, 2007
    The Mandibular ramus morphology (lower jaw bone) on a recently discovered specimen of Australopithecus afarensis closely matches that of gorillas. This finding was unexpected given that chimpanzees are the closest living relatives of humans.,,,its absence in modern humans cast doubt on the role of Au. afarensis as a modern human ancestor.
    http://www.arn.org/blogs/index.....cestral_li

    “The australopithecine (Lucy) skull is in fact so overwhelmingly simian (ape-like) as opposed to human that the contrary proposition could be equated to an assertion that black is white.”
    Lord Solly Zuckerman – Chief scientific advisor to British government and leading zoologist

    Lucy – The Powersaw Incident – (a humorous video showing how biased evolutionists can be with the evidence to ‘make the evidence’ fit their preconceived conclusion)
    http://www.metacafe.com/watch/4032597

    “If pressed about man’s ancestry, I would have to unequivocally say that all we have is a huge question mark. To date, there has been nothing found to truthfully purport as a transitional species to man, including Lucy, since 1470 was as old and probably older. If further pressed, I would have to state that there is more evidence to suggest an abrupt arrival of man rather than a gradual process of evolving”.
    Richard Leakey, world’s foremost paleo-anthropologist, in a PBS documentary, 1990.
    http://www.wasdarwinright.com/earlyman.htm

  10. continued rebut on human evolution:

    The supposed next step for ‘human evolution’ does not fair any better for the evolutionists than Lucy did:

    The changing face of genus Homo – Wood; Collard
    Excerpt: the current criteria for identifying species of Homo are difficult, if not impossible, to operate using paleoanthropological evidence. We discuss alternative, verifiable, criteria, and show that when these new criteria are applied to Homo, two species, Homo habilis and Homo rudolfensis, fail to meet them.
    http://www3.interscience.wiley.....0/abstract

    Human evolution?
    Excerpt: Some scientists have proposed moving this species (habilis) out of Homo and into Australopithecus (ape) due to the morphology of its skeleton being more adapted to living on trees rather than to moving on two legs like H. sapiens.
    http://en.wikipedia.org/wiki/H.....Genus_Homo

    Who Was Homo habilis—And Was It Really Homo? – Ann Gibbons – June 2011
    Abstract: In the past decade, Homo habilis’s status as the first member of our genus has been undermined. Newer analytical methods suggested that H. habilis matured and moved less like a human and more like an australopithecine, such as the famous partial skeleton of Lucy. Now, a report in press in the Journal of Human Evolution finds that H. habilis’s dietary range was also more like Lucy’s than that of H. erectus, which many consider the first fully human species to walk the earth. That suggests the handyman had yet to make the key adaptations associated with our genus, such as the ability to exploit a variety of foods in many environments, the authors say.
    http://www.sciencemag.org/cont.....70.summary

    New findings raise questions about who evolved from whom
    Excerpt: The old theory was that the first and oldest species in our family tree, Homo habilis, evolved into Homo erectus, which then became us, Homo sapiens. But those two earlier species lived side-by-side about 1.5 million years ago in parts of Kenya for at least half a million years,,, The two species lived near each other, but probably didn’t interact with each other, each having their own “ecological niche,” Spoor said. Homo habilis was likely more vegetarian and Homo erectus ate some meat, he said. Like chimps and apes, “they’d just avoid each other, they don’t feel comfortable in each other’s company,” he said.
    http://www.msnbc.msn.com/id/20178936/

    The Truth About Human Origins:
    Excerpt: “It is practically impossible to determine which “family tree” (for human evolution) one should accept. Richard Leakey (of the famed fossil hunting family from Africa) has proposed one. His late mother, Mary Leakey, proposed another. Donald Johanson, former president of the Institute of Human Origins in Berkeley, California, has proposed yet another. And as late as 2001, Meave Leakey (Richard’s wife) has proposed still another.,,”
    http://books.google.com/books?.....8;lpg=PT28

    Is the early history of the human race such a mess that it shouldn’t be taught in school? – June 2011
    http://www.uncommondescent.com.....in-school/

    Here are some fairly good videos for refuting the ‘non-skeptical’ hypothesis of human evolution:

    Human Evolution? – What Do The Bones Really Say? – Don Patton – video
    http://www.youtube.com/watch?v=NEw8fk6NvbI

    Human Evolution ? – Dr. Marc Surtees – Video
    http://edinburghcreationgroup......lution.xml

    Is There a Monkey in Your Family Tree ? – Thomas Kindell – video
    http://uk.video.yahoo.com/watch/2377111

  11. continued rebut on human evolution:

    This following quote, by a leading evolutionist in the field, is candid in its admission of the gaps for the evidence of human evolution.

    A 2004 book by leading evolutionary biologist Ernst Mayr stated that “The earliest fossils of Homo, Homo rudolfensis and Homo erectus, are separated from Australopithecus (Lucy) by a large, unbridged gap. How can we explain this seeming saltation? Not having any fossils that can serve as missing links, we have to fall back on the time-honored method of historical science, the construction of a historical narrative.”
    Misrepresentations of the Evidence for Human Evolutionary Origins:
    http://www.evolutionnews.org/2......html#more

    Even though the preceding comment from a leading evolutionist in the field is crushing, to the smooth transition needed for the materialist to make his case for human evolution, you would think a materialist would at least have some sort of evidence he could cling to with the Homo erectus and the Homo rudolfensis fossils Mayr alluded to. Yet when we look at the evidence presented by the materialists themselves, for the proposed evolution of Homo Rudolfensis and erectus, the evidence is anything but straight forward and appears to be, once again, ‘shoehorned’ to fit their preconceived philosophical bias:

    “Dr. Leakey produced a biased reconstruction (of 1470/ Homo Rudolfensis) based on erroneous preconceived expectations of early human appearance that violated principles of craniofacial development,” Dr. Timothy Bromage
    http://www.geneticarchaeology......lieved.asp

    Hominids, Homonyms, and Homo sapiens – 05/27/2009 – Creation Safaris:
    Excerpt: Homo erectus is particularly controversial, because it is such a broad classification. Tattersall and Schwartz find no clear connection between the Asian, European and African specimens lumped into this class. “In his 1950 review, Ernst Mayr placed all of these forms firmly within the species Homo erectus,” they explained. “Subsequently, Homo erectus became the standard-issue ‘hominid in the middle,’ expanding to include not only the fossils just mentioned, but others of the same general period….”. They discussed the arbitrariness of this classification: “Put together, all these fossils (which span almost 2 myr) make a very heterogeneous assortment indeed; and placing them all together in the same species only makes any conceivable sense in the context of the ecumenical view of Homo erectus as the middle stage of the single hypervariable hominid lineage envisioned by Mayr (on the basis of a much slenderer record). Viewed from the morphological angle, however, the practice of cramming all of this material into a single Old World-wide species is highly questionable. Indeed, the stuffing process has only been rendered possible by a sort of ratchet effect, in which fossils allocated to Homo erectus almost regardless of their morphology have subsequently been cited as proof of just how variable the species can be.” By “ratchet effect,” they appear to mean something like a self-fulfilling prophecy: i.e., “Let’s put everything from this 2-million-year period into one class that we will call Homo erectus.” Someone complains, “But this fossil from Singapore is very different from the others.” The first responds, “That just shows how variable the species Homo erectus can be.”
    http://creationsafaris.com/cre.....#20090527a

    The ‘selling’ of shoddy evidence is shameless by neo-Darwinists:

    Icon Of Evolution – Ape To Man – The Ultimate Deception – Jonathan Wells – video
    http://vimeo.com/19080087

    Hominid Hype and the Election Cycle – Casey Luskin – September 2011
    Excerpt: Ignoring fraudulent fossils like Piltdown man, the last 50 years have seen a slew of so-called human ancestors which initially produced hype, and were later disproven.
    http://www.evolutionnews.org/2.....50801.html

    But perhaps the most underhanded thing for Mr. Matzke and other ‘unskeptical’ neo-Darwinists to do, is to completely ignore the fact they have demonstrated ‘mechanism’ for body plan morphogenesis, thus they are not even really ‘doing science’ in the first place, but are merely making conjectures with no basis to reality in which to refer to:

    Stephen Meyer – Functional Proteins And Information For Body Plans – video
    http://www.metacafe.com/watch/4050681

    Dr. Stephen Meyer comments at the end of the preceding video,,,

    ‘Now one more problem as far as the generation of information. It turns out that you don’t only need information to build genes and proteins, it turns out to build Body-Plans you need higher levels of information; Higher order assembly instructions. DNA codes for the building of proteins, but proteins must be arranged into distinctive circuitry to form distinctive cell types. Cell types have to be arranged into tissues. Tissues have to be arranged into organs. Organs and tissues must be specifically arranged to generate whole new Body-Plans, distinctive arrangements of those body parts. We now know that DNA alone is not responsible for those higher orders of organization. DNA codes for proteins, but by itself it does insure that proteins, cell types, tissues, organs, will all be arranged in the body. And what that means is that the Body-Plan morphogenesis, as it is called, depends upon information that is not encoded on DNA. Which means you can mutate DNA indefinitely. 80 million years, 100 million years, til the cows come home. It doesn’t matter, because in the best case you are just going to find a new protein some place out there in that vast combinatorial sequence space. You are not, by mutating DNA alone, going to generate higher order structures that are necessary to building a body plan. So what we can conclude from that is that the neo-Darwinian mechanism is grossly inadequate to explain the origin of information necessary to build new genes and proteins, and it is also grossly inadequate to explain the origination of novel biological form.’ – Stephen Meyer – (excerpt taken from Meyer/Sternberg vs. Shermer/Prothero debate – 2009)

    A few comments on Quantum ‘non-local’ epigenetic information:
    https://docs.google.com/document/pub?id=1iNy78O6ZpU8wpFIgkILi85TvhC9mSqzUSE_jzbksoHY

    It should be pointed that this ‘non-local’ (beyond space and time) epigentic information, is very, very, friendly to Theistic postulations for human origins, to put it mildly:
    music and verse:

    Steven Curtis Chapman – God is God (Original Version) -
    http://www.youtube.com/watch?v=qz94NQ5HRyk

    Genesis 2:7
    the LORD God formed the man from the dust of the ground and breathed into his nostrils the breath of life, and the man became a living being.

  12. further notes:

    These following studies, though of materialistic bent, offer strong support that Humans are extremely unique in ‘advanced information capacity’ when compared to animals:

    Darwin’s mistake: Explaining the discontinuity between human and nonhuman minds:
    Excerpt: There is a profound functional discontinuity between human and nonhuman minds. We argue that this discontinuity pervades nearly every domain of cognition and runs much deeper than even the spectacular scaffolding provided by language or culture can explain. We hypothesize that the cognitive discontinuity between human and nonhuman animals is largely due to the degree to which human and nonhuman minds are able to approximate the higher-order, systematic, relational capabilities of a physical symbol system.
    http://www.bbsonline.org/Prepr.....eprint.htm

    Origin of the Mind: Marc Hauser – Scientific American – April 2009
    Excerpt: “Researchers have found some of the building blocks of human cognition in other species. But these building blocks make up only the cement footprint of the skyscraper that is the human mind”,,,
    http://www.wjh.harvard.edu?/~m.....dSciAm.pdf

    Earliest humans not so different from us, research suggests – February 2011
    Excerpt: Shea argues that comparing the behavior of our most ancient ancestors to Upper Paleolithic Europeans holistically and ranking them in terms of their “behavioral modernity” is a waste of time. There are no such things as modern humans, Shea argues, just Homo sapiens populations with a wide range of behavioral variability.
    http://www.physorg.com/news/20.....umans.html

    Geometric Principles Appear Universal in Our Minds – May 2011
    Excerpt: Villagers belonging to an Amazonian group called the Mundurucú intuitively grasp abstract geometric principles despite having no formal math education,,, Mundurucú adults and 7- to 13-year-olds demonstrate as firm an understanding of the properties of points, lines and surfaces as adults and school-age children in the United States and France,,,
    http://www.wired.com/wiredscie.....-geometry/

    These following studies highlight the difficulty materialists have in fitting our mental abilities into any plausible evolutionary scenario:

    New Caledonian Crows Exceed Apes/Chimps at Trap-tube Experiment – video
    http://www.youtube.com/watch?v=M52ZVtmPE9g

    Origin of Soulish Animals:
    Excerpt: Bolhuis and Wynne contrast the cognitive capacities of birds and primates.,,, Evidently, certain bird species exhibit greater powers of the mind than do apes.
    http://www.reasons.org/OriginofSoulishAnimals

    A scientist looks again at Project Nim – Trying to teach Chimps to talk fails
    Excerpt: “The language didn’t materialize. A human baby starts out mostly imitating, then begins to string words together. Nim didn’t learn. His three-sign combinations – such as ‘eat me eat’ or ‘play me Nim’ – were redundant. He imitated signs to get rewards. I published the negative results in 1979 in the journal Science, which had a chilling effect on the field.”
    http://www.arn.org/blogs/index.....roject_nim

    It is also interesting to point out that the materialistic philosophy has an extremely difficult time assigning any proper value to humans in the first place, i.e. Just how do you derive value for a person from a philosophy that maintains transcendent values are illusory?:

    How much is my body worth?
    Excerpt: The U.S. Bureau of Chemistry and Soils invested many a hard-earned tax dollar in calculating the chemical and mineral composition of the human body,,,,Together, all of the above (chemicals and minerals) amounts to less than one dollar!
    http://www.coolquiz.com/trivia...../worth.asp

    Whereas Theism, particularly Christianity, has no trouble whatsoever figuring out how much humans are worth:

    John 3:16
    “For God so loved the world that he gave his one and only Son, that whoever believes in him shall not perish but have eternal life.

    Casting Crowns – Who am I? with lyrics
    http://www.youtube.com/watch?v=Pt7OZyBj5Ik

  13. It leaves us with two kinds of people. Those who pretend to know all the answers, and those who would like to find out as much as possible, incrementally, through research.

    The difference is not that one kind knows and the other kind doesn’t know. The difference is in how one deals with not knowing.

  14. Further notes refuting supposed human evolution:

    Here is a paper which, though technical, shows that the modern genetic evidence we now have actually supports Adam and Eve. Moreover, the evidence it presents from the latest genetic research is completely inexplicable to neo-Darwinism, i.e. neo-Darwinism, once again, completely falls apart upon scrutiny; (and although I don’t agree with the extreme 6000 year Young Earth model used as a starting presumption in the paper for deriving the graphs, the model, none-the-less, can be amended quite comfortable to a longer time period. Which I think provides a much more ‘comfortable’ fit to the overall body of evidence)

    The Non-Mythical Adam and Eve! – Refuting errors by Francis Collins and BioLogos
    http://creation.com/historical-adam-biologos

    CMI has a video of the preceding paper entitled, ‘Are All From Adam and Eve?’ by Dr. Carter. It is at the bottom of the list of videos, on the following site, after you click on the ‘Creation Super Conference link at the bottom of the page:

    ‘Are All From Adam and Eve?’ by Dr. Carter
    http://www.biblediscoverytv.com/

    As well, there is now other lines of compelling ‘Genetic Adam and Genetic Eve’ evidence. This genetic evidence strongly supports the Biblical view of the sudden creation of man as these following videos and article clearly show:

    Human Evolution? – The Compelling Genetic Evidence For Adam and Eve
    Dr. Fazale Rana – video
    http://www.metacafe.com/watch/4284482

    Dr. Fazale Rana defends the integrity of the genetic evidence for Adam and Eve, on page 4 of the following site, from some pretty high level criticism from BioLogos:

    Were They Real? The Scientific Case for Adam and Eve by Fazale Rana – November 2010
    http://www.reasons.org/files/e.....010-04.pdf

    Further note:

    Human Evolution – Genetic Adam And Eve – Hugh Ross – video
    http://www.metacafe.com/watch/4036776

    The “Eve” Mitochondrial Consensus Sequence – John Sanford
    Excerpt: Given the high mutation rate within mitochondria and the large geographic separation among the individuals within our dataset, we did not expect to find the original human mitochondrial sequence to be so well preserved within modern populations. With the exception of a very few ambiguous nucleotides, the consensus sequence clearly represents Eve’s mitochondrial DNA sequence.
    http://www.icr.org/article/mit.....-sequence/

    further notes:

    Chimps are not like humans – May 2004
    Excerpt: the International Chimpanzee Chromosome 22 Consortium reports that 83% of chimpanzee chromosome 22 proteins are different from their human counterparts,,, The results reported this week showed that “83% of the genes have changed between the human and the chimpanzee—only 17% are identical—so that means that the impression that comes from the 1.2% [sequence] difference is [misleading]. In the case of protein structures, it has a big effect,” Sakaki said.

    Chimp chromosome creates puzzles – 2004
    Excerpt: However, the researchers were in for a surprise. Because chimps and humans appear broadly similar, some have assumed that most of the differences would occur in the large regions of DNA that do not appear to have any obvious function. But that was not the case. The researchers report in ‘Nature’ that many of the differences were within genes, the regions of DNA that code for proteins. 83% of the 231 genes compared had differences that affected the amino acid sequence of the protein they encoded. And 20% showed “significant structural changes”. In addition, there were nearly 68,000 regions that were either extra or missing between the two sequences, accounting for around 5% of the chromosome.,,, “we have seen a much higher percentage of change than people speculated.” The researchers also carried out some experiments to look at when and how strongly the genes are switched on. 20% of the genes showed significant differences in their pattern of activity.
    http://www.nature.com/news/199.....524-8.html

    Study Reports a Whopping “23% of Our Genome” Contradicts Standard Human-Ape Evolutionary Phylogeny – Casey Luskin – June 2011
    Excerpt: For about 23% of our genome, we share no immediate genetic ancestry with our closest living relative, the chimpanzee. This encompasses genes and exons to the same extent as intergenic regions. We conclude that about 1/3 of our genes started to evolve as human-specific lineages before the differentiation of human, chimps, and gorillas took place. (of note; 1/3 of our genes is equal to about 7000 genes that we do not share with chimpanzees)
    http://www.evolutionnews.org/2.....47041.html

    Could Chance Arrange the Code for (Just) One Gene?
    “our minds cannot grasp such an extremely small probability as that involved in the accidental arranging of even one gene (10^-236).”
    http://www.creationsafaris.com/epoi_c10.htm

  15. Nick Matzke:

    1. Evolution isn’t a chance process. Natural selection is an anti-chance, nonrandom process. That’s why it’s called “selection”.

    Umm there isn’t any selecting going on Nick and Larry Moran tells us:

    The explanation that best fits the data tells us that >99% of all evolutionary change is due to random genetic drift and not natural selection.

    Nick sez:

    2. Evolution is about the evolution of populations and species. The special features of individuals, particularly rare individuals like Mozart, require additional explanation.

    More standard nonsensical propaganda- Populations tend to reign in deviants

    Nick:

    3. Evolution gets you to stone-age humans.

    Yeah if you started with stone-age humans.

    4. We know evolution happened because we have the fossils which show it happening.

    Unfortunately you require biological/ genetic evidence that demonstrates the transformations required are possible. And to date you don’t have that.

    IOW your “fossils” are just a matter of “If I didn’t believe it I wouldn’t have seen it.”

    So Nicjk how can we test your claim that your view of the fossils is the correct one?

  16. That’s one of biggest LsOC I’ve heard. To know that not knowing is preferable to knowing requires knowing. Rather self defeating if you ask me.

    Not knowing is what it is. We don’t know and can’t say. Knowing leads us to two things – 1) more knowledge – 2) the knowledge that we have a lot more to learn.

    It’s really a false humility to assume that someone who has (or claims to have) a particular knowledge is not being realistic with what he/she does not know.

    So there’s two kinds of people, I agree. But the two kinds are those who are wrong and those who are right, and those two types have branches if rightness and wrongness. Deciphering through all that is right and wrong is our task.

    Materialism to the unbiased observer appears at the outset to be irrational, and it gets worse the more one looks into it.

    DrBot below has led him/herself into the obvious corner with materialism. Once there the arguments get even more irrational. Don’t believe me? Pay attention to how he/she responds (if he/she responds) to my last post there. The point where a materialist realizes that infinite regresses of causes are absurd, is the point where irrational explanations for existence begin – such as multiverses and what have you. I fully expect him/her to start going there.

    All the research in all of space and time is not going to magically transfer him/her or you out of that corner. It’s not so much a matter of knowing or not knowing, but a matter of primary logic when one thinks rationally about how and why we exist. It’s that primary logic that has led us to the strength of mind to be able design, engineer and assemble great things, and to learn about our world to the extent we have. It didn’t begin with the research, but with right reason. Materialism is the absolute antithesis to right reason on it’s very face.

  17. 17
    material.infantacy

    “It leaves us with two kinds of people. Those who pretend to know all the answers, and those who would like to find out as much as possible, incrementally, through research.”

    I agree. Pretending to know that there is a material root to the biological tree is question begging. It’s much better to keep the origins question open to inquiry, allowing for any logical possibilities to be illuminated by evidence.

    The difference is not that one kind knows and the other kind doesn’t know. The difference is in how one deals with not knowing.

    Exactly. It makes no sense to assume a cause that has not been shown to be in effect, considering that the cause is at issue. Let’s instead be reasonable and follow the evidence where it leads.

    Well said.

  18. Why people keep saying that evolutionists think that Mozart happened “by chance”?

    We don’t.

  19. Joseph: >99% ~= all.

    Moreover, what that 99% tells us is there are a huge number of mutations that are near-neutral in the current environment.

    This is extremely important.

  20. 20
    material.infantacy

    By necessity then — or is there another primary causal mechanism that doesn’t “emerge” from chance and necessity?

  21. I don’t know how you want to parse it into “Chance” and “Necessity” – I don’t find them a very useful pair of concepts myself, but by the simple logical fact that if things replicate with heritable variation, and at least some of that variation is variation in reproductive success, the population will adapt to its environment.

  22. Why do you think events must be either chance OR necessity? Why can’t events happen due to processes that combine chance AND necessity, as we observe in biological evolution?

  23. Joseph, Intelligent Design is NOT Anti-Evolution! The fossil record shows clear signs of evolution, but that doesn’t mean the deep time evolutionary patterns we see weren’t directed by God.

    I wish you ID skeptics would get this straight for once.

  24. 24
    material.infantacy

    Information imparted by the environment is restricted to the constraints imposed by the anthropic principle, AFAICT — apart from that you have the laws of physics acting on material substances, varying stochastically within the physical constraints also imposed by the anthropic principle.

    At the very least, Mozart is a necessity based on conditions established with the very cause directly preceding the introduction of time and space. That is to say, a necessity given enough probabilistic resources — and so, the product of chance and necessity, dependent upon the constraints within which C/N operates, i.e., the anthropic principle.

    The only primary cause that apparently can be added to chance and necessity, in a material framework, is that which was imposed at the genesis of the universe: the physical constraints that allow for material laws in the first place. Other causes, it would seem, are secondary, or “emergent” given the previous assumptions.

  25. I know ID is not anti-evolution. I also know we can have evolution and not have universal common descent.

    I know we can have natural selection, ie evolution, and not have ucd.

  26. It is exteremely important to expose the impotence of Nick’s claims.

  27. chance and necessity- they said “and”

  28. Elizabeth:

    Why people keep saying that evolutionists think that Mozart happened “by chance”?

    Well it definitely ain’t on purpose on by plan or by design. So what is left?

    Reproductive success? Many things contribute to that, including the loss of functionality.

    And guess what? There isn’t any evidence that demonstrates reproductive success can account for the appearance of new, useful and functional multi-part systems.

  29. 29
    material.infantacy

    Adding to the above point: even in a strict chance and necessity framework, the laws themselves are contingent and specific. Hence, information is primary to all that exists, and to everything determined from the genesis of time and space.

  30. Joseph, you’re not making any sense here. First you said

    “Umm there isn’t any selecting going on”

    then you said

    “I know we can have natural selection, ie evolution”

    You have directly contradicted yourself in the span of two posts.

  31. Elizabeth:

    It’s strange how darwinists sometimes have to rephrase things in order to make them apparently more credible, at least to themselves.

    Let’s be clear: the neodarwinian algorithm is made of chance and necessity. There is no other way to describe it.

    Chance and necessity are, moreover, completely separated in the algorithm.

    Chance is the RV part. RV is the only engine of variation, the only tool for generating new functional information.

    Necessity is the NS part. Positive NS acts only after RV has generated new information that is naturally selectable, and its only effectis to expand the new information in the population.

    On the other hand, negative NS has the role of “protecting” the information that already exists.

    These fundamental points should be clear to all. They cannot be forgotten.

    When dariwnists say that NS is not random, they are saying a half truth. It is true that it is not random: it is a necessity algorithm.

    But, at the same time, it is certainly not teleologic. As I have said many times, it is indeed wrong to call it “selection” at all. It is not the environment that selects anything. The environment just is what it is, and determines certain variables, that are not in any way connected to the information in biological beings. Again, it’s the replicating process that really selects the best replicators, given the current environment.

    NS is a byproduct of the replicating process, and of the information already present in the replicators, that allows them to replicate.

    The only generator of new information, however, in the neodarwinian process, is RV. In essence, the darwinian peocess is a random process, with possible amplification at certain steps, if and when positively naturally selectable functional information appears (that is, practlcally never).

    So, let’s say it’s mud to Mozart by chance, with possible little help at some crucial steps. Nonsense, just the same.

  32. What do we really observe? The odds of (a combination of) chance and necessity as a cause of the existing or extinct forms of life are laughably small. It is not serious science. It is make-believe science.

  33. 33

    Umm there isn’t any selecting going on Nick and Larry Moran tells us:

    The explanation that best fits the data tells us that >99% of all evolutionary change is due to random genetic drift and not natural selection.

    Larry Moran is talking about the genomes of humans and other large genomes and how much of the sequence change is under selection vs. neutral. Most of it is thought to be neutral. Amongst other things, this is strong evidence that a lot of these large genomes is junk (another position which Moran argues for).

    This is nothing like saying that “there isn’t ANY selecting going on” — Moran doesn’t believe that and neither does anyone else in biology. It also doesn’t mean anything about the evolution of phenotype — body size, shape, etc. All of that can be under strong selection, and still 99% of the genome changes (but not all of them) on the sequence level can be neutral. Only a few percent of the genome is even coding sequence or regulatory anyway.

    The fact that you don’t know these obvious points, and instead rely on misinterpretation of a quote mine, and no one in your camp has corrected you here or elsewhere, is, yet again, yet another huge, crashing reason why scientists are digusted by creationists and rightly so.

  34. Umm “natural selction” is just differential reproduction due to heritable random variation- nothing is being selected as whatever works good enough gets by.

  35. Nick,

    Nature does not select and whatever works good enough survives and reproduces. You cannot look at the genomes of individuals in a population and tell which is going to outreproduce the others. You cannot tell by looking at the organism- natural selection is an after-the-fact statistical assessment.

    As for “strong selection”, well we see that when humans are involved, for example in infections when anti-biotics are used. The surviving bacteria are those with loss-of-function mutations which isn’t the type of change your position requires.

    The fact that YOU don’t know these obvious points, and instead rely on bullying and spewage, is, yet again, yet another huge, crashing reason why most people are disgusted with evotard “scientists”.

  36. And BTW Nick- the way you use the word creationist it seems to mean “someone who adheres to the evidence and thinks imagination is best left to bedtime stories”.

  37. It’s strange how darwinists sometimes have to rephrase things in order to make them apparently more credible, at least to themselves.

    Well, I bed to differ! I keep “rephrasing things” because from where I’m standing it looks as though people consistently misunderstanding it, and it’s so simple! So I keep trying to find a phrasing that well get that simplicity across!

    Let’s be clear: the neodarwinian algorithm is made of chance and necessity. There is no other way to describe it.

    Of course there is. It’s terrible way to describe it – it tells you virtually nothing. Both terms beg a great may questions, and even if you defined them extremely precisely, that still wouldn’t tell you how what the algorithm is. And, btw, it’s not a “neodarwinian algorithm” – it’s the algorithm that Darwin himself proposed. The entire field of evolutionary biology has grown hugely and elaborated hugely since Darwin’s time, not least because Darwin had no idea what the mechanisms of inheritance and variance creation were, and one of the hugely important developments has been an appreciation of the role of drift. But Darwin’s algorithm still lies at the heart of evolutionary theory, and if you want to critique it, you have to understand precisely what it is!”Chance and Necessity” is about as helpful as “food and drink” in describing a healthy diet. Actually less helpful, because the terms themselves have very broad meanings.

    Chance and necessity are, moreover, completely separated in the algorithm.

    No, they aren’t.

    Chance is the RV part. RV is the only engine of variation, the only tool for generating new functional information.

    “Random variation” is not a “tool” at all. It’s a result. And “random” isn’t even a terribly good description – “stochastic” would be better. Variants are not drawn from a flat distribution: genotypic variants that result in phenotypes that are similar to the parent are much more common than variants give rise to very different phenotypes. Moreover, there is no reason why the basic Darwinian algorithm cannot work at the level of population level as well as at the organism level, so that populations that have reproductive mechanisms that tend to give rise to optimal mutation rates and optimal kinds of mutations will tend be better able to adapt to changing environments and therefore tend to have longer-lasting lineages than populations with less optimal variance-generating mechanisms. And there is growing evidence for this, for example in DNA repair mechanisms, and, indeed, the evolution of sexual reproduction and, with it, genetic recombination mechanisms, which not only generate useful variety, but also allow alleles to propagate independently through the population. So in these senses, variation is not “random” – there are perfectly good causal mechanisms (“necessity”) for mutations, and some may have actually evolved at population level, because they confer greater adaptability on the population.

    Necessity is the NS part. Positive NS acts only after RV has generated new information that is naturally selectable, and its only effectis to expand the new information in the population.

    Well, Natural selection is stochastic too. And to say “its only effect is to expand the new information in the population” does not do justice to what happens. Better to drop the agency language altogether. “NS” doesn’t “act” at all. Again, it’s a result – a direct result of heritable variation in reproductive success. But it’s highly stochastic, in that what determines whether an individual breeds or not includes many many factors that have nothing to do with its genotype, and one result of this is “drift” – near neutral mutations can propagate through the population almost as readily as slightly beneficial ones. This means that any population is constantly being drip-fed by near-neutral mutations, while ones that confer less-than-average chance of survival in the current environment tend to become less prevalent, and ones that confer more-than-average chance tend to become more prevalent. And a population with rich genetic variation is going to be more adaptable should some permanent shift in environmental conditions come along.

    On the other hand, negative NS has the role of “protecting” the information that already exists.

    Again, you have been misled by your figure of speech. There aren’t two kinds of NS. NS itself is a figure of speech only. What there are are variants that tend to promote better-than-average reproduction in the current environmente and variants that tend toe promote worse-than-average ditto, plus of course many many variants that don’t do anything other than make life more interesting. However, change the environment ever so slightly (and the allele frequency in the population is itself an environmental factor, so there is lots of feedback going on here, and therefore lots of non-linearities) and what was once beneficial may become neutral or deleterious, and what was once deleterious may become neutral or beneficial. So rather than “NS expanding or protecting information”,what is happening is that the environment is leaving behind, in the population gene pool, a record of what works or worked in that environment.

    These fundamental points should be clear to all. They cannot be forgotten.

    They are far from clear, and are very misleading.

    When dariwnists say that NS is not random, they are saying a half truth. It is true that it is not random: it is a necessity algorithm.

    No, for reasons I have give above. Dawkins gets this very wrong, btw.

    But, at the same time, it is certainly not teleologic. As I have said many times, it is indeed wrong to call it “selection” at all. It is not the environment that selects anything. The environment just is what it is, and determines certain variables, that are not in any way connected to the information in biological beings. Again, it’s the replicating process that really selects the best replicators, given the current environment.

    No, it’s the environment that does the selection (if you insist on agency language). The replication process merely “offers” the environment variants from which to select. If the environment thinks that a white individual doesn’t deserve to replicate, it sends an owl to eat it. If it thinks that a nice brown individual deserves to breed, it hides it from the owl. I jest of course – but that’s the kind of mess you get into with agency language, and is certainly more accurate than the idea that the replication process does the selecting! Except of course in the case of sexual selection, but that one helps my case not yours!

    NS is a byproduct of the replicating process, and of the information already present in the replicators, that allows them to replicate.

    Yes, exactly, it’s a byproduct. And of course you are correct that information already present allows them to replicate. Without that basic function there can be no Darwinian evolution, which is why Darwinian evolution can’t explain how the first self-replicators got started. But there’s a heck of a lot more to the information in the genome than simply the information required to replicate. There’s information about how to forage, how to avoid being prey, etc, and all that information gets there from environment, which “selects” those variants that solve these problems.

    Or rather, because this language produce more heat than light, once you have a self-replicating mechanism that results in replication with heritable variance in reproductive success, those variants that replicate best in the current environment will come to dominate the population. That’s the Darwinian algorithm, and it’s dead simple.

    The only generator of new information, however, in the neodarwinian process, is RV. In essence, the darwinian peocess is a random process, with possible amplification at certain steps, if and when positively naturally selectable functional information appears (that is, practlcally never).

    Trying to separate “RV” from “NS” is bootless, IMO. And trying to attribute “information creation” to one half rather than the other, is even more pointless. Apart from the prerequisite that the population must be able to replicate, the “information” that accrues in the population genotypes over time is just as much a product of the variance-creation processes as it is a product of the “selection” process, as should be apparent if instead of thinking of the Darwinian mechanism as “RM+NS” as so many people write it,you think of it as what it is: a single mechanism: self-replication with heritable variance in reproductive success. If there is no variance-producing mechanism in the reproductive process there will be no accumulation of information; but equally, if the variance that is produced has no effect on reproductive success, there won’t be any accumulation of information either. Both are necessary; neither is sufficient.

    So, let’s say it’s mud to Mozart by chance, with possible little help at some crucial steps. Nonsense, just the same.

    And I hope it is clear from my post that this is indeed, nonsense, and not proposed by anyone :)

  38. How do you compute the odds for the outcome of a long term feedback process like the empirically observed process of reproduction without knowing a detailed history of each step of the process?

    Can you provide a sample calculation? I’d really like to see the math behind this remarkable claim.

  39. Right, how can one compute odds on something that has never been shown to even be feasible?

  40. Joseph:

    Right, how can one compute odds on something that has never been shown to even be feasible?

    I see we agree that the “it’s too improbable to have evolved” argument is worthless.

    What do you suggest we do to stop ID proponents from using such a meaningless and unsupportable argument?

  41. Joseph:

    Umm “natural selction” is just differential reproduction due to heritable random variation- nothing is being selected as whatever works good enough gets by

    Joseph, working good enough to get by is defined as being naturally selected.

    Do you really not understand such a basic concept?

  42. Nick,

    Just another creationists with uninformed emotional objections, rather than real ones.

    I am not a “creationists,” and my objections have nothing to do emotion. I am a real scientist, who follows the evidence where it leads, unlike Darwinists who make up stories and call it science.

    Natural selection throws out failed experiments. It has no creative power whatsoever.

    Here’s an unvarnished presentation of the Darwinian-materialistic fairytale, which you would have us accept on “scientific authority”:

    Once upon a time, the physical universe came into existence. No one has any idea why or how, but it must have been just an accident.

    The laws of physics that originated at the birth of the universe seem to be finely-tuned to permit the evolution of a life-permitting universe, but it must have been just an accident.

    Once upon a time, inanimate matter spontaneously generated the first self-replicating cell. No one has any idea how this could have happened, but we have faith: it must have been just an accident.

    Then random errors and natural selection eventually produced everything we observe in biology, from the information-processing machinery of the cell to the mind of Mozart.

    We realize that many people might not buy this line of argumentation, but we are scientists. Trust us. We have it all figured out, except for some minor details, which we’ll get to later.

    This is what you are trying to sell Nick. Good luck.

  43. GilDodgen:

    Natural selection throws out failed experiments. It has no creative power whatsoever.

    If NS throws out failed experiments, then it must keep successful experiments, right?

    Natural selection by itself has no creative power, agreed.

    New natural ‘experiments’ by themselves have no creative power.

    However, the combined processes of experiments vetted by natural selection and used as a basis for subsequent generations are observed to create any number of new morphological and behavioral variations.

    Why shouldn’t the combined processes of keeping the successful results for reuse count as being creative?

  44. corrected links:

    Bones Of Contention – Dr. Marc Surtees – video
    http://edinburghcreationgroup.org/video/20

    Is there a Monkey in your Family Tree? – Thomas Kindell – video
    http://www.youtube.com/watch?v=OWu96RQe6Mo

  45. Gino you state:

    keeping the successful results for reuse count as being creative

    Okie Dokie Gino, let’s look for some ‘successful results’ to see if we can make this whole neo-Darwinian thing work:

    notes:

    Where’s the evidence for Darwinism?

    Many of these researchers also raise the question (among others), why — even after inducing literally billions of induced mutations and (further) chromosome rearrangements — all the important mutation breeding programs have come to an end in the Western World instead of eliciting a revolution in plant breeding, either by successive rounds of selective “micromutations” (cumulative selection in the sense of the modern synthesis), or by “larger mutations” … and why the law of recurrent variation is endlessly corroborated by the almost infinite repetition of the spectra of mutant phenotypes in each and any new extensive mutagenesis experiment (as predicted) instead of regularly producing a range of new systematic species…
    (Wolf-Ekkehard Lönnig, “Mutagenesis in Physalis pubescens L. ssp. floridana: Some Further Research on Dollo’s Law and the Law of Recurrent Variation,” Floriculture and Ornamental Biotechnology Vol. 4 (Special Issue 1): 1-21 (December 2010).)
    http://www.evolutionnews.org/2.....42191.html

    Four decades worth of lab work is surveyed here:

    “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain – Michael Behe – December 2010
    Excerpt: In its most recent issue The Quarterly Review of Biology has published a review by myself of laboratory evolution experiments of microbes going back four decades.,,, The gist of the paper is that so far the overwhelming number of adaptive (that is, helpful) mutations seen in laboratory evolution experiments are either loss or modification of function. Of course we had already known that the great majority of mutations that have a visible effect on an organism are deleterious. Now, surprisingly, it seems that even the great majority of helpful mutations degrade the genome to a greater or lesser extent.,,, I dub it “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain.
    http://behe.uncommondescent.co.....evolution/

    Michael Behe talks about the preceding paper in this following podcast:

    Michael Behe: Challenging Darwin, One Peer-Reviewed Paper at a Time – December 2010
    http://intelligentdesign.podom.....3_46-08_00

    How about the oft cited example for neo-Darwinism of antibiotic resistance?

    List Of Degraded Molecular Abilities Of Antibiotic Resistant Bacteria:
    Excerpt: Resistance to antibiotics and other antimicrobials is often claimed to be a clear demonstration of “evolution in a Petri dish.” ,,, all known examples of antibiotic resistance via mutation are inconsistent with the genetic requirements of evolution. These mutations result in the loss of pre-existing cellular systems/activities, such as porins and other transport systems, regulatory systems, enzyme activity, and protein binding.
    http://www.trueorigin.org/bacteria01.asp

    That doesn’t seem to be helping! How about we look really, really, close at very sensitive growth rates and see if we can catch almighty evolution in action???

    Unexpectedly small effects of mutations in bacteria bring new perspectives – November 2010
    Excerpt: Most mutations in the genes of the Salmonella bacterium have a surprisingly small negative impact on bacterial fitness. And this is the case regardless whether they lead to changes in the bacterial proteins or not.,,, using extremely sensitive growth measurements, doctoral candidate Peter Lind showed that most mutations reduced the rate of growth of bacteria by only 0.500 percent. No mutations completely disabled the function of the proteins, and very few had no impact at all. Even more surprising was the fact that mutations that do not change the protein sequence had negative effects similar to those of mutations that led to substitution of amino acids. A possible explanation is that most mutations may have their negative effect by altering mRNA structure, not proteins, as is commonly assumed.
    http://www.physorg.com/news/20.....teria.html

    Shoot that doesn’t seem to be helping either! Perhaps we just got to give the almighty power of neo-Darwinism ‘room to breathe’? How about we ‘open the floodgates’ to the almighty power of Darwinian Evolution and look at Lenski’s Long Term Evolution Experiment and see what we can find after 50,000 generations, which is equivalent to somewhere around 1,000,000 years of human evolution???

    Richard Lenski’s Long-Term Evolution Experiments with E. coli and the Origin of New Biological Information – September 2011
    Excerpt: The results of future work aside, so far, during the course of the longest, most open-ended, and most extensive laboratory investigation of bacterial evolution, a number of adaptive mutations have been identified that endow the bacterial strain with greater fitness compared to that of the ancestral strain in the particular growth medium. The goal of Lenski’s research was not to analyze adaptive mutations in terms of gain or loss of function, as is the focus here, but rather to address other longstanding evolutionary questions. Nonetheless, all of the mutations identified to date can readily be classified as either modification-of-function or loss-of-FCT.
    (Michael J. Behe, “Experimental Evolution, Loss-of-Function Mutations and ‘The First Rule of Adaptive Evolution’,” Quarterly Review of Biology, Vol. 85(4) (December, 2010).)
    http://www.evolutionnews.org/2.....51051.html

    Now that just can’t be right!! Man we should really start to be seeing some neo-Darwinian fireworks by 50,000 generations!?! Hey I know what we can do! How about we see what happened when the ‘top five’ mutations from Lenski’s experiment were combined??? Surely now the Darwinian magic will start flowing!!!

    Mutations : when benefits level off – June 2011 – (Lenski’s e-coli after 50,000 generations)
    Excerpt: After having identified the first five beneficial mutations combined successively and spontaneously in the bacterial population, the scientists generated, from the ancestral bacterial strain, 32 mutant strains exhibiting all of the possible combinations of each of these five mutations. They then noted that the benefit linked to the simultaneous presence of five mutations was less than the sum of the individual benefits conferred by each mutation individually.
    http://www2.cnrs.fr/en/1867.htm?theme1=7

    Now something is going terribly wrong here!!! Tell you what, let’s just forget trying to observe evolution in the lab, I mean it really is kind of cramped in the lab you know, and now let’s REALLY open the floodgates and let’s see what the almighty power of neo-Darwinian evolution can do with the ENTIRE WORLD at its disposal??? Surely now almighty neo-Darwinian evolution will flex its awesomely powerful muscles and forever make those IDiots, who believe in Intelligent Design, cower in terror!!!

    A review of The Edge of Evolution: The Search for the Limits of Darwinism
    The numbers of Plasmodium and HIV in the last 50 years greatly exceeds the total number of mammals since their supposed evolutionary origin (several hundred million years ago), yet little has been achieved by evolution. This suggests that mammals could have “invented” little in their time frame. Behe: ‘Our experience with HIV gives good reason to think that Darwinism doesn’t do much—even with billions of years and all the cells in that world at its disposal’ (p. 155).
    http://creation.com/review-mic.....-evolution

    Michael Behe, The Edge of Evolution, pg. 162 Swine Flu, Viruses, and the Edge of Evolution
    “Indeed, the work on malaria and AIDS demonstrates that after all possible unintelligent processes in the cell–both ones we’ve discovered so far and ones we haven’t–at best extremely limited benefit, since no such process was able to do much of anything. It’s critical to notice that no artificial limitations were placed on the kinds of mutations or processes the microorganisms could undergo in nature. Nothing–neither point mutation, deletion, insertion, gene duplication, transposition, genome duplication, self-organization nor any other process yet undiscovered–was of much use.”
    http://www.evolutionnews.org/2.....20071.html

    Now, there is something terribly wrong here! After looking high and low and everywhere in between, we can’t seem to find the almighty power of neo-Darwinism anywhere!! Shoot we can’t even find ANY power of neo-Darwinism whatsoever!!! It is as if the whole neo-Darwinian theory, relentlessly sold to the general public as it was the gospel truth, is nothing but a big fat lie!!!

  46. Nature does not select- I understand the concept and the concept says nothing is being selected. Eliminated, perhaps- is that what yo are talking about? Selected for elimination? “individuals of lower fitness are removed from the population”- ernst mayr in “what evolution is”

    You do realize that is all that is happening, right? Or do you not really understand the concept?

    Darwin called it “natural selection” because he wanted to trick people into thinking is was like artificial selection. But some caught on and that is where “survival of the fittest” comes in.

  47. Insufficient probabilistic resources, beyond trivialities.

  48. Right, until someone shows it is even feasible we shouldn’t talk about probabilities.

    But until evos stop using worthless promissory notes and imagination, instead of actual evidence, then we are most likely stuck with probability arguments. But hey at least those give you the benefit of the doubt.

  49. GilDodgen:

    Insufficient probabilistic resources, beyond trivialities.

    I’ll ask the same questions I asked of Eugene:

    How do you compute the probability for the outcome of a long term feedback process like the empirically observed process of reproduction without knowing a detailed history of each step of the process?

    It’s one thing to claim insufficient probabilistic resources, it’s quite another to actually demonstrate such insufficiency. Merely computing a number for a feature’s existing composition without taking into account its history is a basic beginner’s error in probability calculations.

    Even Joseph, who seems to be an ardent ID supporter, agrees such probability calculations cannot be done.

  50. Joseph

    Nature does not select- I understand the concept

    Apparently you don’t understand, because in scientific terminology ‘naturally selected’ doesn’t imply ‘consciously and positively chosen’. It merely means ‘survived in its environment long enough to reproduce’

    It will be difficult if not impossible to have any meaningful discussion if you won’t use the scientifically accepted definition and insist on your own made-up one.

  51. Elizabeth:

    With all the respect I have for you, I think it was not necessary for you to give immediately such a good example of the truth of my previous statement:

    “It’s strange how darwinists sometimes have to rephrase things in order to make them apparently more credible, at least to themselves.”

    You say:

    Well, I bed to differ! I keep “rephrasing things” because from where I’m standing it looks as though people consistently misunderstanding it, and it’s so simple! So I keep trying to find a phrasing that well get that simplicity across!

    My only comment could be: well, you seem to have succeeded in “make them apparently more credible to yourself”.

    For the rest, you go on with amazing examples of wrong reasoning. I will try to point at least at some of them, possibly showing how the “rephrasing strategy” takes place.

    Of course there is. It’s terrible way to describe it – it tells you virtually nothing. Both terms beg a great may questions, and even if you defined them extremely precisely, that still wouldn’t tell you how what the algorithm is.

    Let’s see…

    And, btw, it’s not a “neodarwinian algorithm” – it’s the algorithm that Darwin himself proposed.

    I refer to the “neodarwinian algorithm” because all my debates are exactly about that, the “modern synthesis”, as it was proposed about 60 years ago, with the application to darwinian thought of the new understanding of molecular biology. As practically all ny arguments are based on molecular biology, the neodarwinian model is my target, and I try to call it with its correct name.

    The entire field of evolutionary biology has grown hugely and elaborated hugely since Darwin’s time, not least because Darwin had no idea what the mechanisms of inheritance and variance creation were, and one of the hugely important developments has been an appreciation of the role of drift.

    Exactly my point.

    But Darwin’s algorithm still lies at the heart of evolutionary theory, and if you want to critique it, you have to understand precisely what it is!

    I do. And the darwinian model is applied very literally in neodarwinian thought.

    Chance and Necessity” is about as helpful as “food and drink” in describing a healthy diet. Actually less helpful, because the terms themselves have very broad meanings.

    In this phrase, there is almost all the bad strategy of some darwinists (alas, including you). A bad metaphor (food and drink). A completely wrong statement (chance and necessity have very specific meanings, food and drink are instead broad categories). And no support at all of what is being said.

    Just to differ, I give specific definitions of “chance” and “necessity”.

    We call a “necessity system” one where the evolution of the system can be explicitly described with deterministic laws, and computed, with a reasonable level of precision.

    We call a “random system” one where we are not able to do that, but we can still describe rather well the evolution of the system by the application of some appropriate probability function.

    I believe those meanings are very specific, and defined.

    No, they aren’t.

    Yes, they are. Just to differ, I try to explain why.

    Given the definitions above, we can describe the RV part as a random system, and the NS part as a necessity system.

    So, the generation of new information in an existing population (or, if you prefer, pool of populations) is exclusively a random system (RV), and it happens in very long times, in absence of any necessity mechanism controlling it. That’s exactly the reason why neutral evolution, including genetic drift, are completely random systems.

    But, as soon as NS can act (and it can act only if naturally selectable information has already been generated by the random system of RV), it acts in short times according to necessity laws, favouring the expansion of the new information (positive NS), and protecting the existing functional information (negative NS).

    More in next post.

  52. Elizabeth:

    “Random variation” is not a “tool” at all. It’s a result.

    About your problems with the “agency” terminology. I can agree, it is not the best. I just take it from the darwinists. The concept of “engine of variation” is not mine. You don’t like “tool”, it’s fine for me. But “result” is probably not good too, at least for RV. Well, in the end the variation is a result, but the random system that produces it is certainly a specific system, and we know well enough the details of that system, and the details and causes of most forms of random variation (single point mutations, indels, shuffling, and so on). Anyway, I agree that we can call the final result “RV”, and describe it as the result of a random system.

    “Random variation” is not a “tool” at all. It’s a result. And “random” isn’t even a terribly good description – “stochastic” would be better.

    From Wikipedia:

    “Stochastic (from the Greek ?????? for aim or guess) refers to systems whose behaviour is intrinsically non-deterministic. A stochastic process is one whose behavior is non-deterministic, in that a system’s subsequent state is determined both by the process’s predictable actions and by a random element. However, according to M. Kac[1] and E. Nelson,[2] any kind of time development (be it deterministic or essentially probabilistic) which is analyzable in terms of probability deserves the name of stochastic process.”

    So, what’s the problem with you? Why the useless rephrasing?

    OK, do you want me to call the whole neodarwinian algorithm “stochastic” instead of saying that it includes a random part and a necessity part? Fine. The whole neodarwinain algorithm is stochastic. And its random component (RV) is a random system. We have rephrased.

    Variants are not drawn from a flat distribution: genotypic variants that result in phenotypes that are similar to the parent are much more common than variants give rise to very different phenotypes.

    Here is a serious error of thought.

    I will state it explicitly: a random system is any system well described by a probability distribution, whatever it is.

    I am not sure what you mean with the term “flat distribution”, but I suppose you mean a uniforma distribution. Well, I have ro remind you that it is not necessary, at all, that the distribution be uniform to call a random system a random system. Indeed, most random systems in nature do not have a uniform distribution. So, what’s your point here?

    genotypic variants that result in phenotypes that are similar to the parent are much more common than variants give rise to very different phenotypes.

    Yes. And it’s a random system all the same. It’s called a random walk.

    Moreover, there is no reason why the basic Darwinian algorithm cannot work at the level of population level as well as at the organism level, so that populations that have reproductive mechanisms that tend to give rise to optimal mutation rates and optimal kinds of mutations will tend be better able to adapt to changing environments and therefore tend to have longer-lasting lineages than populations with less optimal variance-generating mechanisms.

    And so? Is that an argument against the random nature of variation? Is random variation in a pool of populations less random? I must be missing something.

    And there is growing evidence for this, for example in DNA repair mechanisms, and, indeed, the evolution of sexual reproduction and, with it, genetic recombination mechanisms, which not only generate useful variety, but also allow alleles to propagate independently through the population.

    Here I have lost you completely. Are you saying something?

    So in these senses, variation is not “random” – there are perfectly good causal mechanisms (“necessity”) for mutations, and some may have actually evolved at population level, because they confer greater adaptability on the population.

    There are always “perfectly good causal mechanisms” in any random system, ingluding the toss of a coin (you know, newton mechanics…). That does not make the systems less random. Random systems are not “non deterministic systems”, otherwise the only random systems would be at quantum level, and all our texts about probability, with their coins and dies, would be wrong.

    And it’s not the “causal mechanisms” that “evolve”. The causal mechanisms are always the same, and they can be traced to the necessity laws of physics and biochemistry. What “evolves” is the information pattern on which those causal mechanisms act. And, if it evolves by a neodarwinian algorithm (twhich I don’t believe), then it is by RV and NS, again.

    More in next post.

  53. Elizabeth:

    Well, Natural selection is stochastic too.

    Why? Once there is a reproductive advantage, expansion takes place. That is a necessity mechanism. OK, it’s not as definite as a law of physics, and some random effects must be taken into consideration too. But that has nothing to do with the RV that generaes the selectable information.

    So, let’s say that the NS part is a necessity system, with some random components. OK?

    And to say “its only effect is to expand the new information in the population” does not do justice to what happens.

    Why? The only effect of positive NS is exactly that. What other effects are you aware of?

    Better to drop the agency language altogether.

    Again, I take the agency language from current darwinain thought. I am very happy to drop it.

    “NS” doesn’t “act” at all. Again, it’s a result – a direct result of heritable variation in reproductive success.

    OK. It’s a result. The result of a specific necessity law: what reprodusces better, reproduces better. The law “acts”, and it produces results. I think I would keep the verb “act” for necessity laws, but if you prefer to say that logical and causal laws are a result of something, please let me know.

    But it’s highly stochastic, in that what determines whether an individual breeds or not includes many many factors that have nothing to do with its genotype

    Correct. See above. There is a random component in the NS part, but it has nothing to do with the randomness in RV. But it’s the necessity part in NS which is important to the algorithm. But if you want, you can add the random components in NS to the probabilistic resources of the system. It changes nothing.

    and one result of this is “drift” – near neutral mutations can propagate through the population almost as readily as slightly beneficial ones.

    I have already discussed that with you. Drift is a random source of variation. It has nothing to do with NS (nothing is selected in drift). And it does not change the probabilities of a random walk.

    This means that any population is constantly being drip-fed by near-neutral mutations, while ones that confer less-than-average chance of survival in the current environment tend to become less prevalent, and ones that confer more-than-average chance tend to become more prevalent.

    IOWs, in any population RV and NS are sequencially acting. Where is the news? Please, do not object to “sequencially”. It means that NS can only act on the products of RV. Do you deny that?

    And a population with rich genetic variation is going to be more adaptable should some permanent shift in environmental conditions come along.

    OK. But a population rich in genetic variation can also be weaker. Too much variation is a very dangerous thing.

    More in the next post.

  54. So in one case you have a thing that eternally exists, and causes the universe to exist, and in the other case you have a thing that eternally exists, and causes the universe to exist. But in one of those two cases there is an absurdity of an infinite regress of causes …

    Can you explain why?

  55. Elizabeth:

    Again, you have been misled by your figure of speech.

    Let’s see.

    There aren’t two kinds of NS.

    Yes, there are. Please, read any biological literature, and you will see.

    Positive selection applies to variation confers a reproductive advantage, and usually favours the expansion of the new trait in a population.

    Negative selection just eliminates variation which confers a reproductive disadvantage, and keeps the already existing important functional sequences “as pure as possible” in the course of evolution.

    They are two different mechanisms, that apply to different things.

    NS itself is a figure of speech only.

    Like all words, and concepts. A figure of speech of which there are two different kinds.

    If you want, I can rephrase:

    There is a figure of speech called positive NS, and another figure of speech called negative NS. Happier?

    What there are are variants that tend to promote better-than-average reproduction in the current environmente and variants that tend toe promote worse-than-average ditto, plus of course many many variants that don’t do anything other than make life more interesting.

    IOWs (I beg your pardon, in other figures of speech, IOFOS) there is positive NS, begative NS, and neutral variation, to which no selection applies. Where’s the news?

    However, change the environment ever so slightly (and the allele frequency in the population is itself an environmental factor, so there is lots of feedback going on here, and therefore lots of non-linearities) and what was once beneficial may become neutral or deleterious, and what was once deleterious may become neutral or beneficial.

    That’s correct, and again trivial. The important point is: changes in the environment are random in respect to biological information. They have no “added information” about how proteins work, or what molecular changes are more likely to give adaptation. That’s what I mean when I say that the environment is blind to life (Petrushka, are you ready to intervene with the ususal aggressions?)

    So rather than “NS expanding or protecting information”,what is happening is that the environment is leaving behind, in the population gene pool, a record of what works or worked in that environment.

    Talk of “agency language”!

    Positive NS expands information. A functional protein is a functional protein, whatever the environment shift that may have “helped” select it. The information for an enzyme expands only if the enzyme works. So, positive NS expands only functional information.

    Negative NS eliminates strongly non functional information. A non functional protein, if incompatible with life, not only does not expand, but is canceled form the population, because the individual bearing ir dies. In most cases, it dies not because of some shift in environment, but simply because the mutated protein is incompatible with the general working of the organism.

    Your “agency language” smart rephrasing does not change the facts.

    More in next post.

  56. Elizabeth:

    They are far from clear, and are very misleading.

    There is no doubt they are far from clear for you.

    No, for reasons I have give above. Dawkins gets this very wrong, btw.

    You have given where?

    And for once, I stick with Dawkins: there are many things ge gets very wrong, but the neodarwinain algorithm is not one of them.

    No, it’s the environment that does the selection (if you insist on agency language).

    I absolutely don’t insist on agency language. And you?

    So, let’s say that nothing does the selection. Least of all the environment. :)

    The replication process merely “offers” the environment variants from which to select.

    Agency language. Double.

    I jest of course

    Wohw! For a moment I thought you were serious!

    is certainly more accurate than the idea that the replication process does the selecting!

    Why? Let’s say that the result is mainly a result of the reproduction process, given a certain environment. You see, no agency language here, and still I am in a mess! :) It must be something uncurable in my genome…

    If a protein that is basci for DNA transcription mutates and does not work anynore, and the individual dies and cannot reproduce, that is negative NS. What has the environment to do with it?

    If a new light sensitive domains emerges, and let’s say it is the first step to vision, it is a new useful function anyway, and it could be naturally selectable in many different environments. (OK, if no light exists, it will not be selected). But the main reason why it is selected is that is works, it detects light. The function is the main reason of selection. True, in some environments that function will not be useful, and will not be selected. In most, it will be.

    So, let’s say that NS is the result of at least three components: the function to be selected, the reprouction process, and the existing environment.

    More in next post.

  57. Elizabeth:

    Yes, exactly, it’s a byproduct. And of course you are correct that information already present allows them to replicate. Without that basic function there can be no Darwinian evolution, which is why Darwinian evolution can’t explain how the first self-replicators got started.

    Hey. We agree for three consecutive phrases! That’s something. :)

    But there’s a heck of a lot more to the information in the genome than simply the information required to replicate. There’s information about how to forage, how to avoid being prey, etc,

    Mmmhhh… OK.

    and all that information gets there from environment, which “selects” those variants that solve these problems.

    No. Here we have to disagree again.

    First of all, let’s drop the agency.

    “all that information gets there from environment, and is the result of the better reproduction in that environment of those variants that solve these problems.”

    It is wrong just the same. The information in no way “gets there from the environment”. What logic is that?

    The information gets there from RV. And expands because it solves problems in the environment (or for any other reason that can give a reproductiove advantage).

    Why cannot you admit this very simple point?

    Let’s say that the function that expands is a new protein that confers an advantage. Penicillinase could be a good example. A complex and very efficient enzyme, that allows bacteria to grow even in the presence of penicillin. What better example of a positive selction strongly grounded in the environment?

    And yet, how can you say that “that information gets there from environment”? Does environment know the sequence of penicillinase?

    The simple truth is: environment is totally blind to the information that is necessary to build a penicillinase molecule. A very complex, very functional information (beta-lactamases are usually about 300 AAs long).

    The simple truth is that positive NS can only act to expand a penicillinase gene only after the molecular information is already there, in the gene. And where did that information come from (at least, according to the neo-darwinain model?): from RV. (In the same way, negative NS can only fix an already functional gene).

    So, the only way to state it is:

    “all that information gets there from random variation, and its expansion and fixation is the result of the better reproduction in that environment of those randomly generated variants that solve these problems.”

    Is that OK?

    Or rather, because this language produce more heat than light, once you have a self-replicating mechanism that results in replication with heritable variance in reproductive success, those variants that replicate best in the current environment will come to dominate the population. That’s the Darwinian algorithm, and it’s dead simple.

    IOWs:

    “once random variation generates a self-replicating mechanism that results in replication with heritable variance in reproductive success, those variants that replicate best in the current environment will come to dominate the population.”

    And so? As you say:

    “That’s the Darwinian algorithm, and it’s dead simple.”

    It’s true. And it’s exactly as I have described it.

    Ah, I forgot: with some rephrasing.

    More in next post.

  58. Elizabeth:

    Trying to separate “RV” from “NS” is bootless, IMO.

    A wrong opinion. I have shown why it is not bootless. It is simply good reasoning.

    And trying to attribute “information creation” to one half rather than the other, is even more pointless.

    It is not pointless. It is simply correct. See my previous post.

    Apart from the prerequisite that the population must be able to replicate, the “information” that accrues in the population genotypes over time is just as much a product of the variance-creation processes as it is a product of the “selection” process

    No. The information is a product of RV, and its accumulation (expansion) is a product of the selection process. You are simply rephrasing it (“the “information” that accrues in the population genotypes over time”) so that the two concept may appear connected to a casual reader. But it does not work.

    As usual, you have problems with the concept of information. Once a functional penicillinase gene arises from RV (well, it can’t, I know: I am just discussing the scenario), the information is all there. The fact that the inforamtion expands in the population does not add to the information, no more than printing 1000 copies of Hamlet adds to the information in the play.

    The problem is that you darwinists refuse to accept the simple, and important, concept of semantic information. And you don’t want to separate hardware from software. And you don’t want to separate RV form NS, and random systems from necessity systems, and so on.

    For pretending to be rational skeptics, you are really a strange bunch of holistic fellows, I must say.

    as should be apparent if instead of thinking of the Darwinian mechanism as “RM+NS” as so many people write it,you think of it as what it is:

    What it is is RV + NS.

    a single mechanism: self-replication with heritable variance in reproductive success.

    Not too much imagination in this rephrasing. Try again. The environment is not even quoted.

    If there is no variance-producing mechanism in the reproductive process there will be no accumulation of information;

    That’s for sure!

    but equally, if the variance that is produced has no effect on reproductive success, there won’t be any accumulation of information either.

    Well, the information will all be there, but it will not expand. Why do you use the word “accumulation” to bypass the problem of the “generation” of information?

    Both are necessary; neither is sufficient.

    Correct.

    RV is necessary and sufficient to generate new functional information (according to the neodarwinain algorithm).

    NS is necessary and sufficient to expand and fix the naturally selectable information that already has been generated.

    The neo-darwinian algorithm is made of both parts. RV + NS.

    Exactly as I have always said.

    And I hope it is clear from my post that this is indeed, nonsense, and not proposed by anyone

    It is nonsense. And it is what is proposed by the neo-darwinian model (even if you seem not to understand it).

    So, I will state it again. According to the neo-darwinian models, it’s:

    Mud to Mozart by chance, with possible little help at some crucial steps.

    Nonsense, just the same.

  59. gpuccio, I have to object here. You say I have misunderstood evolutionary theory.

    I think you should, at the very least, consider that you have misunderstood evolutionary theory, although you are by no means alone on this site. Please re-read my original post more carefully, first suspending the sarcastic voice in your head, and try to respond to my actual comments instead of lampooning them. Perhaps I am wrong (although clearly I don’t think so), but do me the courtesy of entertaining the possiblity that the mistake may be yours.

  60. OK, let’s go right back to basics. No agency language at all, and we will eschew “Chance and Necessity”.

    Let’s start with where we agree:

    Me:

    And of course you are correct that information already present allows them to replicate. Without that basic function there can be no Darwinian evolution, which is why Darwinian evolution can’t explain how the first self-replicators got started.

    So we start with agreement that Darwinian evolution depends on there being an initial population of self-replicators that replicate with heritable variance in reproductive success.

    This means that Darwinian evolution does even attempt to explain “mud to Mozart” but “simplest-possible-population-of-self-replicators-that-replicate-with-heritable-variance-in-reproductive-success to Mozart”.

    Right?

    Please indicate whether you agree with this. But assuming you do, let us continue:

    You seem to complain that in my formulation: “self-replication with heritable variance in reproductive success”, ” The environment is not even quoted”.

    In fact, I have frequently “quoted” the environment, or rather added the additional specifier “in the current environment”, although it is not necessary for the formulation because clearly, the formulation works fine without it, because everything exists in some environment. The point of adding “in the current environment” is that it points out that it is only the current environment that has any influence on what traits enhance reproductive success.

    So the basic Darwinian proposition is as follows:

    “once you have a self-replicating mechanism that results in replication with heritable variance in reproductive success, those variants that replicate best in the current environment will come to dominate the population. ”

    Which you attempt to paraphrase as:

    “once random variation generates a self-replicating mechanism that results in replication with heritable variance in reproductive success, those variants that replicate best in the current environment will come to dominate the population.”

    Which is indeed nonsense. Clearly Darwinian process cannot generate the prerequisites for Darwianin processes! It isn’t what I said, isn’t what I meant, and isn’t what a single evolutionary biologist claims.

    It is a straw man, and your entire critique of Darwinism seems to be predicated on this mistaken understanding of evolutionary theory.

    I’ll stop there, and wait for your response, before tackling the rest of your posts.

  61. Elizabeth:

    I always entertain the possibility that the mistake may be mine. And the possibility that the mistale may be of the other. And I try to decide.

    We both can be wrong. It’s human condition. That’s why arguments, reason and communication are useful. A credible argument can do much more than a reminder of the fragility of human cognition.

    I have discussed in detail why I believe that Dawkins and I are right about evolutionary theory, and you are wrong. I have carefully read all your points, and answered them one by one, in many long posts.

    You can do the same, if you like.

    And believe me, the “sarcastic voice” in my head (and, I hope, in my posts) is not for you. But, certainly, for the ideas you express. The ideas certainly deserve sarcasm, sometimes. I have the greatest respect for you as a person, but that respect implies that I wholly express my reactions to the things you say, good or bad that they are.

  62. Elizabeth:

    First point:

    This means that Darwinian evolution does even attempt to explain “mud to Mozart” but “simplest-possible-population-of-self-replicators-that-replicate-with-heritable-variance-in-reproductive-success to Mozart”.

    Yes and no. The position of many darwinists, of not debating OOL, is wrong. It is obvious that replicators already contain information, and that information had to be generated somehow.

    Now, you believe in some very simple FUCA. That should have come into existence, I believe, only by RV in a non replicating context.

    So, that would be from mud to FUCA by chance alone.

    Then, FUCA becomes LUCA, I suppose, by RV + NS.

    And then LUCA becomes Mozart by RV + NS.

    So, why are you objecting to “mud to Mozart” by RV + NS?

  63. As I’ve got a moment, a word on the “two kinds” of natural selection.

    Again, rather than argue about this, let’s go back to basics, and leave the “selection” terminology out of it.

    We agree, I think (or hope), that “selection” is neither more nor less than “heritable traits with differential reproductive success in a given environment”. Some new variants will have no effect on the phenotype at all. Some new variants will have an effect on the phenotype, but not one that makes any difference to its reproductive success, relative to the average success of its peers. Some will confer greater reproductive success relative to its peers, some lesser.

    In practice most variants are near-neutral in effect on reproductive success, and so the chances of any new variant propagating through the population is heavily dependent on luck.

    However, overall, some of these new variants will tend to be propagated systematically more than others because they tend to produce phenotypes that tend to reproduce more successfully than average in the current environment, and some will be propagated systematicallhy less becauses they tend to result in phenotypes that reproduces less successfully in the current environment. This is necessarily true.

    Thus referring to “two kinds of selection” is potentially misleading IMO, whatever the text books say. There is merely differential reproductive success in the current environment, and what confers better than average reproductive success in one environment may confer less than average reproductive success in another, and vice versa.

    Do you agree with this, and if not, why not?

  64. Elizabeth:

    Which you attempt to paraphrase as: “once random variation generates a self-replicating mechanism that results in replication with heritable variance in reproductive success, those variants that replicate best in the current environment will come to dominate the population.” Which is indeed nonsense. Clearly Darwinian process cannot generate the prerequisites for Darwianin processes! It isn’t what I said, isn’t what I meant, and isn’t what a single evolutionary biologist claims.

    What is nonsense. I really don’t understand your point (if there is a point).

    Let’s see again:

    “once random variation generates a self-replicating mechanism that results in replication with heritable variance in reproductive success”

    Maybe the praphrasing game has generate some misunderstanding. What I mean here is :

    “once random variation generates in a replication population a self-replicating mechanism that results in heritable better replication function, and therefore in reproductive success”

    Is that more clear? And what is your problem with that?

    “those variants that replicate best in the current environment will come to dominate the population”

    I suppose we agree about that.

  65. Elizabeth:

    I agree, but I don’t see the misleading potential. Of course I agree that the word “selection” is not a good one, but it is the one currently used (and not certainly created by us IDists).

    In practice most variants are near-neutral in effect on reproductive success, and so the chances of any new variant propagating through the population is heavily dependent on luck.

    In the standard terminology, neutral or near neutral variation is not cisible to selection. It can propagate or be lost, or just stay in some indivisuals. All that is random variation again.

    However, overall, some of these new variants will tend to be propagated systematically more than others because they tend to produce phenotypes that tend to reproduce more successfully than average in the current environment, .

    Yes. That, in stanbdard terminology, is positive natural selection: the expansion of naturally selectable traits, whose effect is to potentiate (higly, I would say) the probabilistic resources that a naturally selectable trait may be a step to further evolution.

    and some will be propagated systematicallhy less becauses they tend to result in phenotypes that reproduces less successfully in the current environment.

    Yes. That, in stanbdard terminology, is negative natural selection: the elimination of heavily non functional variation, whose effect is to fix existing functional information.

    This is necessarily true.

    That’s why it is called the “necessity part” of the algorithm.

    There is merely differential reproductive success in the current environment

    That is, positive NS and negative NS. And so?

  66. Yes and no. The position of many darwinists, of not debating OOL, is wrong. It is obvious that replicators already contain information, and that information had to be generated somehow.

    The process of self-replication, in some senses of “information”, necessarily involves the transmission of “information” from parent to offspring – in other words, if you look at the offspring of a self-replicator, you can deduce “information” about the parent.

    So, in a fairly trivial sense, yes. And yes, of course, as we agree, Darwinian processes cannot kick in until you have a self-replicator that not only self-replicates but self-replicates with heritable differential reproductive success.

    Now, you believe in some very simple FUCA. That should have come into existence, I believe, only by RV in a non replicating context.

    It makes no sense to talk about “random variation” in a “non replicating context”. In fact, as I have argued, the word “random” itself is an extremely loose one, and potentially misleading. But I readily agree, as would any OOL researcher, that the first self-replicator must have derived from a non-self-replicator. This is necessarily true! What the researchers want to find out is the chemical environment in which the formation of such a self-replicator might have been likely. A “soup” of organic molecules, possible in conjunction with some kind of porous substrate, such as clay, or ice, is one possibility.

    So, that would be from mud to FUCA by chance alone.

    Well, no. “Chance alone” is a meaningless phrase. Is it “chance alone” that determines whether an atom of some isotope will decay? The process is highly stochastic, but also highly predictable, statistically. Given reactive chemicals, their inter-reaction may be virtually inevitable. That doesn’t mean that when it happens is entirely predictable, and it may depend on the presence of some catalyst, or other condition (heat, for instance, or thermocline).

    Then, FUCA becomes LUCA, I suppose, by RV + NS

    Well, the FUCA could be the LUCA. It probably won’t be, though, just as “mitochondrial Eve” was one woman, but won’t forever be the same woman.

    But yes, from the FUCA onwards, the basis of evolutionary theory is that heritable variation in differential reproductive success in the current environment will do the job.

    And then LUCA becomes Mozart by RV + NS.

    Well, so does the FUCA. By means of heritable variation in differential reproductive success in the current environment.

  67. Gotta run now :) Will be back later.

  68. 68

    How do you compute the probability for the outcome of a long term feedback process like the empirically observed process of reproduction without knowing a detailed history of each step of the process?

    If one cannot provide the probability of a theoretical, historical process in producing a currently existing feature, one has no business claiming that it is a fact that the process is responsible for the generation of that feature.

    Unless Darwinists provide an evolutionary metric that describes what RM & NS is (and is not) capable of, the claim that RM & NS can and did produce current evolutionary features is non-falsifiable.

    When Darwinists refuse to provide such a metric, but rather rely on “just so” narratives that assume their conclusion, then skepticism is a proper response.

  69. What is nonsense is the part that says you need random variation before you can get random variation!

    But I think I’m seeing the difficulty: random variation presupposes something that varies. Perhaps you mean “random events generate a self-replicating mechanism, etc.”

    In which case, that’s better, but “random” is still problematic. What do you mean by “random”? Chemistry isn’t “random” in most usages of that word, and, in any case “random” is not a precisely defined word.

    OK, maybe we are getting somewhere! Gotta run again…

  70. Elizabeth:

    Yes, I believe we are getting somewhere. Random events is fine for me.

    Chemistry is not random, but is does not produce self replicating RNA, which I believe is the minimal target for today’s fashionable OOL theories.

    But a random system, evolving by the laws of chemistry, could in theory generate that kind of complex molecules.

    I believe that’s what RNA world fans do believe.

    If the laws of chemistry did generate self-replicating RNA by necessity, we would see that happening all the time.

    The idea is that it happened in long strtches of times, because it is an unlikely output of a random system evolving by chemistry laws.

    Random is a word whose definition is not self-evident, but is is precise just the same.

    I have given you the definition in one of my posts:

    “We call a “necessity system” one where the evolution of the system can be explicitly described with deterministic laws, and computed, with a reasonable level of precision.

    We call a “random system” one where we are not able to do that, but we can still describe rather well the evolution of the system by the application of some appropriate probability function.

    I believe those meanings are very specific, and defined.”

  71. Elizabeth:

    I think you misunderstand OOL theories. Even if a ” “soup” of organic molecules, possible in conjunction with some kind of porous substrate, such as clay, or ice,” could be the most favourable environment for the emergence of life, still that emergence would be a rnadom and unlikely output in that system.

    Just think: maybe we can find a system which with some likelihood can favour the chemical formation of RNA chains (after having in some way favored the formation of the nucleotides). Well, there is probably no such environment, but let’s sy we find it.

    The problem remains of how the right sequence for a self-replicating rNA molecule was generated. That is a random event, and its probability can be computed, because obviously there is no law of chemistry that favours the right sequence.

    Indeed, RNA world promoters have spent a lot of time trying to show that a simple self-replicaint RNA molecule is in the range of the probabilistic resources of a prebiotic environment. I don’t agree, but the fact that they try means that they understand the probabilistic aspect of the problem.

  72. I agree. Darwinism is all about irresponsibly using various figures of speech.

  73. GinoB:

    It merely means ‘survived in its environment long enough to reproduce’

    Right, no selection is taking place. And I am using the scientifically accepted definition of NS. Geez I cited Ernst Mayr, one of the architects of the modern synthesis.

    Then we have:

    “Natural selection is the result of differences in survival and reproduction among individuals of a population that vary in one or more heritable traits.” Page 11 “Biology: Concepts and Applications” Starr fifth edition

    The Origin of Theoretical Population Genetics (University of Chicago Press, 1971), reissued in 2001 by William Provine:

    Natural selection does not act on anything, nor does it select (for or against), force, maximize, create, modify, shape, operate, drive, favor, maintain, push, or adjust. Natural selection does nothing….Having natural selection select is nifty because it excuses the necessity of talking about the actual causation of natural selection. Such talk was excusable for Charles Darwin, but inexcusable for evolutionists now. Creationists have discovered our empty “natural selection” language, and the “actions” of natural selection make huge, vulnerable targets. (pp. 199-200)

  74. I was taught over and over again that the accumulation of random mutations led to evolutionary change — led to new species.-Dr Lynn Margulis

    “Random” means without any plan nor purpose

  75. GP,

    As usual, the nonsense of neo-Darwinism is exposed in a clear and concise way. It stands no scrutiny. Bravo!

  76. William J Murray

    If one cannot provide the probability of a theoretical, historical process in producing a currently existing feature, one has no business claiming that it is a fact that the process is responsible for the generation of that feature.

    What a bizarre claim! Asserting that a historical event didn’t happen because you can’t assign an accurate probability value to it is beyond silly. Any number you could come up with won’t change the positive evidence for the event one iota.

    What was the probability of WW1 happening just the way it did? What was the probability of a 10km asteroid hitting the Earth 65 MYA? Do you really want to claim those things didn’t happen because we can’t assign a probability value?

    If an event has already happened, the probability of it having occurred is 1.0

  77. GinoB:

    Asserting that a historical event didn’t happen because you can’t assign an accurate probability value to it is beyond silly.

    Then it is a good thing that isn’t what he is saying.

  78. Eugene S

    I agree. Darwinism is all about irresponsibly using various figures of speech.

    I notice neither you nor William J Murray nor GilDodgen answered the actual question:

    “How do you compute the probability for the outcome of a long term feedback process like the empirically observed process of reproduction without knowing a detailed history of each step of the process?”

    Do you not know the answer?

  79. Well FIRST one has to demonstrate a feasibility exists. By even trying to compute a probability they are giving your position more than it deserves.

  80. Joseph

    Well FIRST one has to demonstrate a feasibility exists.

    Then you must agree with the following statements, right?

    “Unless ID proponents provide a design metric that describes what ID is (and is not) capable of, the claim that ID can and did produce current biological features is non-falsifiable.

    When ID proponents refuse to provide such a metric, but rather rely on subjective “it looks designed to me” narratives that assume their conclusion, then skepticism is a proper response.”

  81. 81

    GinoB:

    The “event” in question is not, say, that “winged flight” or “sexual reproduction” became existent at some point in history, just as it would not be debated if WWII occurred. That is not the challenge.

    If one is going to claim, however, that it is a fact that X process (RM & NS) is what caused the event to occur, then it is up to those making that claim to demonstrate that X process (RM & NS) at the very least least cannot be ruled out, and should show that X process is at least theoretically (categorically) up to the challenge of generating X.

    Until this falsifiable metric is provided, it can only be a bare hypothesis that process X (RM & NS) is even capable of causing the event (macroevolutionary morphological feature) in question.

    The event is not being questioned; the process that caused the event is.

  82. 82

    “Unless ID proponents provide a design metric that describes what ID is (and is not) capable of, the claim that ID can and did produce current biological features is non-falsifiable.

    When ID proponents refuse to provide such a metric, but rather rely on subjective “it looks designed to me” narratives that assume their conclusion, then skepticism is a proper response.”

    Nobody here (that I’m aware of) is claiming that ID did produce such features as a matter of scientific fact, but rather is only claiming that ID is the best provisional explanation for some features, because the only agency or process we know of that produces well over 500-1000 bits of FSCO/I is intelligent design (that of humans).

    500-1000+ bits of FSCO/I is the ID metric where the “best explanation” of any phenomena moves from “physics & chance” to ID agency. ID is unnecessary to explain FSCO/I below that amount, thus it is falsifiable in terms of the only thing it claims according to the metric it provides: “best provisional explanation”.

    Darwinists, however, claim that RM & NS are what factually generated the features in question, without a means of falsifying it even as “best provisional explanation”.

  83. William J Murray

    If one is going to claim, however, that it is a fact that X process (RM & NS) is what caused the event to occur, then it is up to those making that claim to demonstrate that X process (RM & NS) at the very least least cannot be ruled out, and should show that X process is at least theoretically (categorically) up to the challenge of generating X.

    No one in science claims the theory of evolution is a fact.

    Here is a good description of the difference between the observed fact of evolution and the theory of evolution that explains the observed fact.

    Evolution as Fact and Theory

    It would help considerably if you learned to not confuse the two concepts.

  84. Corrected video link:

    Are All From Adam and Eve

    or

    The Non Mythical Adam and Eve (Dr Robert Carter) – video
    http://www.youtube.com/watch?v=8ftwf0owpzQ

    Here is the related paper which, though technical, shows that the modern genetic evidence we now have actually supports Adam and Eve. Moreover, the evidence it presents from the latest genetic research is completely inexplicable to neo-Darwinism, i.e. neo-Darwinism, once again, completely falls apart upon scrutiny; (and although I don’t agree with the extreme 6000 year Young Earth model used as a starting presumption in the paper for deriving the graphs, the model, none-the-less, can be amended quite comfortable to a longer time period. Which I think provides a much more ‘comfortable’ fit to the overall body of evidence)

    The Non-Mythical Adam and Eve! – Refuting errors by Francis Collins and BioLogos
    http://creation.com/historical-adam-biologos

  85. William J Murray

    500-1000+ bits of FSCO/I is the ID metric where the “best explanation” of any phenomena moves from “physics & chance” to ID agency.

    That would be the FSCO/I metric that no one has rigorously defined, or given an objective way to measure, or calculated for any real world biological objects, right?

    In other words it’s just another way of saying “this looks designed to me” with lots of pseudo-technical jargon added for window dressing.

  86. NickMatze, comment #1. Didn’t want this to get buried underneath the ba77 paste bomb.

    2. Evolution is about the evolution of populations and species. The special features of individuals, particularly rare individuals like Mozart, require additional explanation.

    Please elaborate.

    3. Evolution gets you to stone-age humans. Most of what is interesting after that is not evolution, it’s culture. There was rather a lot of cultural development before you got Mozart. Pretending that “evolution” is supposed to explain stuff like that is just silly. You might as well be annoyed with chemistry for not explaining Mozart.

    No one is annoyed with chemistry because nowhere in its history has an a priori assertion been cemented as unquestionable fact.

    Is natural evolution not supposed to explain why we were neurologically capable of developing such talents? I guess you don’t make the claim that RV+NS lead to the transistion from the Baroque period –> Classical –> Romantic because it is too absurd of a claim for even the most diehard Darwinian. But surely you must say that at some point the capability of such talents was evolved through RV+NS. This becomes even more unbelievable. Not only do you theorize mindless particles following the laws of physics to result in Mozart, but that his talent was made possible by RV+NS several millennia before it was even utilized! Evolution just “hit on” an open-ended mechanism, the human mind, that behaves in a way fundamentally different from any other collection of atoms in the known universe. Believe it or you’re an “IDiot”.

    Call it personal incredulity; I’ll call it completely scientifically unverified.

  87. 87

    That would be the FSCO/I metric that no one has rigorously defined, or given an objective way to measure, or calculated for any real world biological objects, right?

    No. It is rigorously defined, and it can be calculated handily. You can find the definition and reference in the FAQ and Glossary on this site, or by googling “kairosfocus FSCO/I” and finding many exhaustive epxlanations and examples on this site and others.

  88. 88

    “That would be the FSCO/I metric that no one has rigorously defined, or given an objective way to measure, or calculated for any real world biological objects, right?”

    I meant to put the above in blockquote in the above post.

  89. GinoB,

    ID is falsifiable and “it looks designed tio me” is more than enough to check into the possibility, especially when there aren’t any known blind, undirected processes that can account for it.

    Also the design metric for ID is the same as it is for archaeology and forensic science.

  90. 90

    GinoB:

    I have a hypothetical exercise for you:

    If we were to find an object on a newly discovered but otherwise uninteresting, uninhabited, desolate planet, and someone suspected that it might be an intelligently designed object (such as, an acient, crashed, alien spacecraft), how would one go about substantiating their suspicion scientifically?

  91. 91

    Perhaps you should read your own sources. From your link:

    Well, evolution is a theory. It is also a fact.

  92. William J Murray

    No. It is rigorously defined, and it can be calculated handily. You can find the definition and reference in the FAQ and Glossary on this site, or by googling “kairosfocus FSCO/I” and finding many exhaustive epxlanations and examples on this site and others.

    What is the FSCO/I of a house cat?

    Is it more or less than the FSCO/I of an amoeba?

    Can you please walk me through the handily calculated cases above? I Googled “kairosfocus FSCO/I” as you suggested but couldn’t find any real world examples. Thanks!

  93. GinoB-

    Perhaps you could provide us with something from your position that has been rigorously defined, that way we can compare and also it will give us some insight into what you will accept.

    That said FCSI is merely Shannon information (rigorously defined) of a specified complexity (also rigorously defined) that has a function/ meaning.

    But you don’t even need to worry about that. Ya see if you can demonstrate taht blind, undirected chemical processes can create new, useful and functional multi-part systems (wrt biology), then the concept of CSI being a design indicator is blown away.

  94. Also the questions would be:

    Does a house cat contain FSCO/I?

    Does an amoeba contain FSCO/I?

  95. 95

    I didn’t say **I** could calculate it handily. I’m not a biologist, nor am I a mathematician. I’ve just read the material I referred to (and other such material) and I’ve read where kairosfocus and others did it and explained the meaning of the values and the process.

  96. Joseph

    Also the questions would be:

    Does a house cat contain FSCO/I?

    Does an amoeba contain FSCO/I?

    But ID’s claim is that all biological life was designed, so therefore all biological life should contain easily measurable FSCO/I.

    You’ve just directly contradicted yourself again Joseph.

  97. Maybe an easier calculation-

    What was the gain in FSCIO in this evolutionary process:

    ““Cross-species analysis revealed interesting evolutionary paths of how this gene had originated from noncoding DNA sequences: insertion of repeat elements especially Alu contributed to the formation of the first coding exon and six standard splice junctions on the branch leading to humans and chimpanzees, and two subsequent substitutions in the human lineage escaped two stop codons and created an open reading frame of 194 amino acids.”

    20^194, like most of you go for?

    Human-Specific De Novo Protein-Coding Gene Associated with Human Brain Functions, Chuan-Yun Li, Yong Zhang, Zhanbo Wang, Yan Zhang, Chunmei Cao, Ping-Wu Zhang, Shu-Juan Lu, Xiao-Mo Li, Quan Yu, Xiaofeng Zheng, Quan Du, George R. Uhl, Qing-Rong Liu*, Liping Wei*, 2009:

  98. William J Murray

    I didn’t say **I** could calculate it handily. I’m not a biologist, nor am I a mathematician. I’ve just read the material I referred to (and other such material) and I’ve read where kairosfocus and others did it and explained the meaning of the values and the process.

    OK, fair enough. Can you please provide a link to where someone has calculated the FSCO/I of a real-world biological entity then? I did search and can’t find a real world example anywhere.

  99. GinoB,

    You have some issues you need to work through. You have yet to show I have ever contradicted myself. So perhaps you should stat there.

    Not everything that is designed contains FSCO/I and the point of any CSI is- is it present or not- its presence indicates design.

    But you don’t even need to worry about that. Ya see if you can demonstrate that blind, undirected chemical processes can create new, useful and functional multi-part systems (wrt biology), then the concept of CSI being a design indicator is blown away.

  100. 1- was that alleged evolutionary process blind and undirected? How can you tell?

    2- Question-begging

  101. “was that alleged evolutionary process blind and undirected? How can you tell?”

    No evolutionary process can be exhaustively proven to be “blind and undirected.” No process of any kind can. I can’t show that Pat Robertson’s god didn’t cause Katrina or Earthquakes. I can point to the natural explanation for those things, but this doesn’t falsify his religious idead.

    That is why theistic evolution can persist, ID is not a science, and it ultimately ID becomes theistic evolution-like when presented details. Here you are, shown an evolutionary pathway: “insertion of repeat elements…and two subsequent substitutions” that creates a new functional gene. Without a reason why, you call it design. Fine as a personal, theistic evolutionary belief, but not science.

  102. Joseph

    Not everything that is designed contains FSCO/I and the point of any CSI is- is it present or not- its presence indicates design.

    Please walk me through the process of determining whether a house cat or amoeba contain FSCO/I. Please explain how to calculate a FSCO/I value (in bits) for those cases. Please show your calculations and the end results which lead to your conclusion. Thanks!

  103. Thanks for admitting that your position is faith-based and not science.

    ID is science for the very reason it is based on our knowledge of cause and effect relationships and any given design inference can be falsified.

    As for you equivocating “evolutionary pathway” is that an intelligent design evolutionary pathway, a front-loaded evolutionary pathway or a blind watchmaker evolutionary pathway?

  104. Umm we can determine if FSCO/I is present without getting an exact number.

    That said I would sart with the minimal complexity of a minmal living organism- ie the most simple living organism.

    CSI has a lower threshold of 500 bits of specified information. Biological function is a specification.

    Mycoplasma genitalium has 580076 base pairs, which equals 1,160,152 (d’oh) bits of information carrying capacity. Out of that 529477 bp code for proteins, ie functionality. That equals 1,058,954 bits of specified information, which is well above the 500 bit threshold.

    Heck just looking at the number of protein coding genes it is obvious that the 500 bit threshold would be easily surpassed.

    No need to get a perfect number for the organism, the threshold is set.

  105. “Thanks for admitting that your position is faith-based and not science.”

    I think you have intentionally failed to comprehend what I wrote. Childish turn-about. Why not just go with “I’m like rubber, you’re like glue”

    “any given design inference can be falsified.”

    You believe the gene presented above is designed. How would I falsify that? Be specific.

    “As for you equivocating “evolutionary pathway” is that an intelligent design evolutionary pathway, a front-loaded evolutionary pathway or a blind watchmaker evolutionary pathway?”

    None of the words you place before “evolutionary pathway” have any demonstrated scientific meaning. Front-loading has never been demonstrated, and retaining a to-be functional element without selection, in light of what you call genetic entropy seems impossible.

  106. Joseph

    Umm we can determine if FSCO/I is present without getting an exact number.

    That said I would sart with the minimal complexity of a minmal living organism- ie the most simple living organism.

    Then why did you claim to not know if a cat or amoeba contained FSCO/I? You certainly are one confused individual.

    CSI has a lower threshold of 500 bits of specified information. Biological function is a specification.

    No. A specification is a document prepared before a design is done outlining the requirements that need to be met. Measuring the physical attributes or function of an object after you discover it does not constitute a specification. You’re painting the bulls-eye around an existing bullet hole and claiming a direct hit.

  107. 107

    From a blog post on this site: “ID Foundations, 5: Functionally Specific, Complex Organization and associated Information as empirically testable (and recognised) signs of design” by kairosfocus, just under the illustration of the ribosome:

    Here, we see a ribosome in action, with the mRNA digitally coded tape triggering successive amino acid additions to the growing protein, as tRNA “taxi” molecules lock to the successive three-letter genetic code codons, and then serving as position-arm devices with the loaded AA’s, that click together. This, until a stop codon triggers cessation and release of the protein. That protein is then folded, perhaps agglomerated with other units, possibly activated and put to work in [or out of] the cell.

    On a simple calculation, since each base in the mRNA has four possible states, the three-letter codon has 4^3 = 64 possible values, as are assigned in the standard D/RNA codon table (or its minor variants). 500 bases, or just under 170 codons, is beyond the 1,000 bit storage capacity threshold.

    A typical protein is about 300 base pairs, and there are thousands in most life forms.

    So, if we trust the sign of FSCO/I, we have good reason to infer that he living cell as we observe it is a designed entity.

    I’m sure you’ll agree that what is being illustrated is a “real world biological entity”.

    Please note that the context of this FSCO/I calculation (the “Foundations of ID” series) is a very in-depth set of articles that exhaustively explain the scientific basis, definitions, history, and qualifications for the validity of the FSCO/I metric.

  108. I love how, in a single post, Nick uses several different meanings of “evolution” — the key to the rhetorical narrative being to see all of reality as a single process of “evolution,” an idea that is very fixed in the Darwinist mind. Once we break out of that intellectual straight-jacket and realize that there is a big difference between change over time, the alleged mechanism of natural selection, descent of man, the blind watchmaker thesis, and other meanings of “evolution,” we can start to have a more nuanced discussion.

  109. 109

    No evolutionary process can be exhaustively proven to be “blind and undirected.”

    Nobody is asking for anyone to “exhaustively prove” that any evolutionary process is blind and undirected; what is being asked is that one demonstrate that blind and undirected processes are categorically capable of producing what they are claimed to have produced with the resources (including time) theorized to be available.

  110. I should also point out that mutation and transposon insertion appear completely random with respect to need when empirically tested in the lab or inferred from sequence.

  111. I just did that. See the reference at 24.

    Processes, which appear random with respect to need (not directed) when tested in the laboratory, or inferred from sequence comparison, created a new protein of 194 amino acids.

  112. So, a protein of 194 amino acids-

    Is that 20^194?

    Or 194 X 3 bases/codon X 2 bits per base = 1164, which is > 500 bits?

  113. They appear random because of our ignorance.

    A transposon has in it sections of DNA that encode two of the enzymes it needs to carry out its job. The cell itself contributes the other necessary enzymes. The motion of these genetic elements about to produce the above mutations has been found to be a complex process and we probably haven’t yet discovered all the complexity. But because no one knows why they occur, many geneticists have assumed they occur only by chance. I find it hard to believe that a process as precise and as well controlled as the transposition of genetic elements happens only by chance. Some scientists tend to call a mechanism random before we learn what it really does. If the source of variation for evolution were point mutations, we could say the variation is random. But if the source of variation is the complex process of transposition, then there is no justification for saying that evolution is based on random events. Dr Lee Spetner “Not By Chance” page 44

    How could you falsify the design inference for the gene you referenced? By demonstrating blind, undirected chemical processes can produce a living organism from non-living matter.

    That is how one falsifies all design inferences by demonstrating agency involvement is not required- ie the event/ object/ structure in question is reducible to matter, energy, chance and necessity.

    Front-loading has never been demonstrated, and retaining a to-be functional element without selection, in light of what you call genetic entropy seems impossible.

    the claims of your position have never been demonstrated and design can and does render the entropy question moot.

    Also I take it that you do not understand that ID is a counter-argument to the blind watchmaker…

  114. GinoB:

    Then why did you claim to not know if a cat or amoeba contained FSCO/I?

    You are certainly confused because I didn’t make that claim.


    CSI has a lower threshold of 500 bits of specified information. Biological function is a specification.

    No.

    Yes.

    A specification is a document prepared before a design is done outlining the requirements that need to be met.

    It doesn’t have to be a document and unless the design mechanism was “POOF”, which it could have been. But other than that given biological function it is a given there was such a specification.

    Measuring the physical attributes or function of an object after you discover it does not constitute a specification.

    OK, no one has seen the documentation for specifying the great pyramids in egypt, the mayan pyramids, etc., etc., etc., but given the complexity of the task at hand and by our measuring the physical attributes of an object after we have discovered it we can be sure that the specifications for those buildings were laid out in advance of their construction.

    Do you understand anything about how science operates?

  115. If the protein arose in an already existing organism then you are begging the question by using what needs to be explained in the first place- namely a living organism.

  116. Joseph

    It doesn’t have to be a document and unless the design mechanism was “POOF”, which it could have been. But other than that given biological function it is a given there was such a specification.

    No, it not a given at all. It is an unsupported assertion on your part that there existed a pre-design specification that needed to be met.

    OK, no one has seen the documentation for specifying the great pyramids in egypt, the mayan pyramids, etc., etc., etc., but given the complexity of the task at hand and by our measuring the physical attributes of an object after we have discovered it we can be sure that the specifications for those buildings were laid out in advance of their construction.

    Actually we have countless examples of pre-design specifications as well as finished products created by humans. That is one of the main ways we can recognize human created designs, by comparing them to other known human created designs. There are no pre-design specifications for biological life.

  117. 117

    Does anyone care to respond to my #22? DrREC? GinoB?

  118. Here’s the basic calc for FSCI. (Notice the further biological cases.) And the Foundation series is here.

  119. Speculation all the way . . . the suggested past is presumed, and the presumed changes are further presumed to be driven by chance and necessity. Circular argument.


  120. It doesn’t have to be a document and unless the design mechanism was “POOF”, which it could have been. But other than that given biological function it is a given there was such a specification.

    No, it not a given at all.

    It is until you can start producing positive evidence for your position. But given the lack of that our current understanding says there was such a specification.

    GinoB:

    Actually we have countless examples of pre-design specifications as well as finished products created by humans.

    Please reference the pre-design specifications for the the great pyramid (egypt- khufu), any mayan pyramid and the buildings at puma punku.

  121. GB, no a specification here is an independent simple description. Biofunction is known to take up a very limited region of possible AA and D/RNA sequence space. That makes the biosequences functionally very specific, Axe’s estimate for proteins on empirical tests is 1 in 10^70 or thereabouts. Comparable to 1 atom to our galaxy.

  122. Which is it?

    What is the fSCI/o of this protein?

    A funny thing here. The falsification of the ID inference is supposed to be showing the gain of functional information in excess of some? value. I did so-by processes which are demonstrably random with respect to need.

    So the proposed falsification of design is, you say, designed. File that away under “why ID isn’t falsifiable.”

    The replies I see:

    1) Call the processes design (With no warrant. They are not correlated to any known design mechanism).

    2) Punt to abiogenesis.

    You guys have anything better?

  123. “the presumed changes are further presumed to be driven by chance and necessity”

    The presumed changes are the result of processes which are demonstrably random with respect to need.

    ID is simply a imposition on top of the data, in this case. You just apply it without any justification.

  124. kairosfocus

    GB, no a specification here is an independent simple description.

    Ah, I see now. What you mean by a specification isn’t the same as the common accepted definition of the word. It’s a term you used to make it sound like there was evidence of pre-planning when in actuality there is no evidence of anything being pre-specified before manufacture.

    Making up your own pet definition then later switching back to the real one is known as equivocation, and is universally frowned upon in scientific community.

  125. Joseph

    Please reference the pre-design specifications for the the great pyramid (egypt- khufu), any mayan pyramid and the buildings at puma punku.

    Construction of the Pyramids

    “Before the physical orientation and layout of a new pyramid took place, considerable planning was needed under the direction of a “royal master builder”. Ultimately, the responsibility fell on the vizier, who was typically the head of all royal works. The first step in the process was taken by specialists who would draw up plans for the pyramid on papyrus. After the construction began, plans and sketches were drawn on papyri or flat slabs of limestone. Planners even made models of their projects, as evidenced by a limestone model of a substructure found in the Pyramid of Amenemhet III at Dahshur. After the planning stage, each step of pyramid building was initiated with foundation rituals.”

    Human designed pyramids had pre-design specifications.

    Where are the pre-design specifications for biological life?

  126. GinoB,

    You are confused. What you posted was the modern rendition of what they think happened. IOW it is your after we discovered it we put together what must have taken place- we did that due to or knowledge of cause and effect relationships.

    Ya see one reason I brought up Puma Punku was because it has been said that the people who built it didn’t have a written language. But given the design that is total nonsense.

    So the bottom line is we can fogure out the specification after the fact.

    But that may be moot because specification wrt biology means “specified to perform a function”- as in not all DNA sequences can produce that effect. So the tighter the variational tolerance the tighter the specification.

    Get it? The more specific the sequence, the tighter the specification.

  127. Joseph

    GinoB, You are confused. What you posted was the modern rendition of what they think happened. IOW it is your after we discovered it we put together what must have taken place- we did that due to or knowledge of cause and effect relationships.

    Joseph, you need to learn how to read.

    Planners even made models of their projects, as evidenced by a limestone model of a substructure found in the Pyramid of Amenemhet III at Dahshur.

    But that may be moot because specification wrt biology means “specified to perform a function”- as in not all DNA sequences can produce that effect.

    No, that is your own pet definition of specification, not one used or accepted by the scientific community. You ID guys can equivocate over your own made up terms all you like, but it will do absolutely nothing to help you get credibility for your claims.

    Now where’s that pre-design specifications for biological life?

  128. GinoB-

    That was one model and it was NOT of the pyramid I asked for.

    Where are the pre-design specifications for Stonehenge? Where are the pre-design specifications for the things I asked about?

    As I said we can, given our knowledge of cause and effect relationships, extrapolate that such a specification existed.

    Now YOU can actually show that to be bogus by doing something other than drooling on your keyboard- that would mean start producing positive evidence for your position.

    Ya see GinoB, once you demonstrate taht blind and undirected chemical prcesses can produce the object/ event/ structure in question then the whole concept of “specification” goes out the window.

    IOW your claims don’t have any credibility.

  129. Dr REC:

    I did so-by processes which are demonstrably random with respect to need.

    It could be random with respect to uranus too but that does not mean it wasn’t directed. Variation within a population is key to the survival of the population. So variation is not random with respect to need as the need is to survive.

    And you still don’t get it- ID is all about ORIGINS because if living organisms were designed then it is a safe bet they were designed to evolve/ evolved by design- meaning your “random with respect to need” is based only on ignorance.

    IOW YOU do not have any warrant calling the process “random”

  130. Joseph

    That was one model and it was NOT of the pyramid I asked for.

    It was an example of the things you say don’t exist. I don’t need to show you every last known case; one is sufficient to falsify your claim.

    Please show me a pre-design specification for any biological life. You don’t have to show them all to make your case, one is quite sufficient.

    As I said we can, given our knowledge of cause and effect relationships, extrapolate that such a specification existed.

    We can use our knowledge of cause and effect relationships for known human designed pyramids to extrapolate that specifications exist for other pyramids. Where is the evidence for a cause/effect relationship for known ‘designed’ biological life?

    Now YOU can actually show that to be bogus by doing something other than drooling on your keyboard

    How wonderfully mature of you.

  131. GinoB:

    It was an example of the things you say don’t exist.

    No it wasn’t. I didn’t say anything about that pyramid.

    I don’t need to show you every last known case; one is sufficient to falsify your claim.

    Wrong again, as usual. All I have to do is show ONE case that we don’t have a pre-design specification for something that had to have had one to support my claim.

    Ya see GinoB, once you demonstrate taht blind and undirected chemical prcesses can produce the object/ event/ structure in question then the whole concept of “specification” goes out the window.

    IOW your claims don’t have any credibility.

  132. Joseph

    It could be random with respect to uranus too but that does not mean it wasn’t directed. Variation within a population is key to the survival of the population. So variation is not random with respect to need as the need is to survive.

    The ‘random’ part of the term ‘random mutation’ by definition means random with respect to its effect on reproductive fitness – either beneficial, deleterious, or neutral. Such changes by definition are completely uncorrelated with ‘need’.

    You inability to understand the simplest terms used by biologists is amazing.

  133. 133

    “It appears random” has no more value than “it appears designed” until someone presents a metric by which one is shown to be more likely than the other given the circumstances in question.

    Without any such metric, one is engaging in speculation. ID theorists provide such a metric; Darwinists do not.

  134. Populations mutating, or with active transposons can be followed over generations, and those mutations sequences.

    When this is done (without selection), the location of mutations and transposon insertion are found to be random with respect to need.

    The mechanisms of each are chemical/physical and understood.

    Random is a statistical metric.

  135. “if living organisms were designed then it is a safe bet they were designed to evolve evolved by design”

    See why this sounds like theistic evolution to me?

    You take a process which is mechanically understood, demonstrably random with respect to need, and best described as evolution.

    You assert that is “design by evolution.” Without adding anything else. Purely superfluous in explanatory power. And identical to theistic evolution.

  136. GinoB 23.2.1

    But ID’s claim is that all biological life was designed, so therefore all biological life should contain easily measurable FSCO/I.

    If you meant that ID claims that every organism is designed, then I would agree with that statement. If that is what you meant, ignore the rest of this. But if you meant that “all of biology” was designed, then read on

    From the “ID Defined” page on this very site. First sentence (emphasis added):

    The theory of intelligent design (ID) holds that certain features of the universe and of living things are best explained by an intelligent cause rather than an undirected process such as natural selection.

    ID does not claim that everything in biology was designed. There are countless biological phenomena that are undeniably stochastic. In fact, I would argue that there is a gradient of items from 100% stochastic to unlikely but possibly stochastic, to probably designed, to so obviously designed that only the deep tugging of an entrenched world view could prevent you from seeing the obvious design.

  137. “In fact, I would argue that there is a gradient of items from 100% stochastic to unlikely but possibly stochastic, to probably designed, to so obviously designed”

    Ok, but it seems like quantitation and a clear rubric for design are essential to ID.

    If you can’t provide either of those, how can you tell designed from undesigned?

  138. 138

    Now, apply that metric to the kind of evolutionary features that are actually being challenged and you’ll have something other than a trivial statement.

  139. William J Murray

    Now, apply that metric to the kind of evolutionary features that are actually being challenged and you’ll have something other than a trivial statement.

    It’s already been done.

    The distribution of fitness effects caused by single-nucleotide substitutions in an RNA virus
    Sanjuán et al
    PNAS June 1, 2004 vol. 101 no. 22 8396-8401

    Abstract: Little is known about the mutational fitness effects associated with single-nucleotide substitutions on RNA viral genomes. Here, we used site-directed mutagenesis to create 91 single mutant clones of vesicular stomatitis virus derived from a common ancestral cDNA and performed competition experiments to measure the relative fitness of each mutant. The distribution of nonlethal deleterious effects was highly skewed and had a long, flat tail. As expected, fitness effects depended on whether mutations were chosen at random or reproduced previously described ones. The effect of random deleterious mutations was well described by a log-normal distribution, with -19% reduction of average fitness; the effects distribution of preobserved deleterious mutations was better explained by a ? model. The fit of both models was improved when combined with a uniform distribution. Up to 40% of random mutations were lethal. The proportion of beneficial mutations was unexpectedly high. Beneficial effects followed a ? distribution, with expected fitness increases of 1% for random mutations and 5% for preobserved mutations.

    and

    The distribution of fitness effects of new mutations
    Eyre-Walker, Keightley
    Nature Reviews Genetics 8, 610-618 (August 2007)

    Abstract: The distribution of fitness effects (DFE) of new mutations is a fundamental entity in genetics that has implications ranging from the genetic basis of complex disease to the stability of the molecular clock. It has been studied by two different approaches: mutation accumulation and mutagenesis experiments, and the analysis of DNA sequence data. The proportion of mutations that are advantageous, effectively neutral and deleterious varies between species, and the DFE differs between coding and non-coding DNA. Despite these differences between species and genomic regions, some general principles have emerged: advantageous mutations are rare, and those that are strongly selected are exponentially distributed; and the DFE of deleterious mutations is complex and multi-modal

    Has ID produced any similar work?

  140. 140

    You cannot look at the genomes of individuals in a population and tell which is going to outreproduce the others.

    Oh, really. Tell that to people who measure the level of drug resistance e.g. in malaria populations.

    You cannot tell by looking at the organism- natural selection is an after-the-fact statistical assessment.

    There are many ways to legitimately infer the action of NS. One is watching it happen. Another is looking at the genomes of populations of organisms for the signatures of selective sweeps. Looking at the genome *is* looking at the organism.

    And, besides, you accept that NS exists and happens, so what the heck are you arguing about?

    Nature does not select and whatever works good enough survives and reproduces.

    Way to dance away from your original argument based on Larry Moran’s quote. Be a man, be a scientist, and admit you made a mistake. Why should or other scientists take you seriously, if you can’t do that?

    As for “strong selection”, well we see that when humans are involved, for example in infections when anti-biotics are used. The surviving bacteria are those with loss-of-function mutations which isn’t the type of change your position requires.

    This is only sometimes true, and often repaired by selection of additional compensatory mutations.

    And besides, *everything* that is an adaptation has a cost on some other criterion. Is flying beneficial for birds? You might think this is a simple question with the answer “yes”, but birds often evolve flightlessness on islands without predators. But you don’t see creationists going around saying “flying isn’t the kind of change the evolutionary position requires, because flight has a large cost that reduces reproductive rate lower than it would otherwise be.” Yet they brazenly use that exact same logic without a second thought when it comes to antibiotic resistance. Creationism = making up ad hoc excuses for ignoring the evidence.

    The fact that YOU don’t know these obvious points, and instead rely on bullying and spewage, is, yet again, yet another huge, crashing reason why most people are disgusted with evotard “scientists”.

    Hmm, name-calling? So much for Christian behavior.

  141. 141

    Please elaborate.

    That’s what the cultural point was, elaboration.

    No one is annoyed with chemistry because nowhere in its history has an a priori assertion been cemented as unquestionable fact.

    Heh, you should google the history of “atomism”. Lots and lots of religious people used to be annoyed by it because they thought it was rank materialism. Eventually they got over it.

    Is natural evolution not supposed to explain why we were neurologically capable of developing such talents?

    Not except in the most generic way. Evolution can explain how we got huge brains, extreme sociality and tool use, etc. What happens after that is cultural use of these basic traits is thousands of years of cultural accumulation, eventually making Mozart possible.

    And even here, it’s not as if *everyone* in the human population can be Mozart. It’s probably a once-in-a-million thing, or less. In any large population measured on any particular criterion (running speed, height, IQ, musical ability), there will be a nice broad bell-curve of the trait, with a few people being really bad, a few people being really good, and a large number being mediocre. This occurs for both cultural and genetic reasons. Presumably if Mozart had been born in the stone age he wouldn’t have been a musical genius.

    Anyway, it’s absurd to take someone from the extreme end of bell-curve and pretend that that’s what evolution “has” to explain. There will be any number of weird individuals at the extremes of any large and diverse population. Evolution is mostly about explaining the population mean. The weird cases have special, local, explanations that probably have precious little to do with the general features that evolution explains.

    Evolution explains why most people have 2 arms and 2 legs. The fact that a few people don’t is not explained by evolution, it is explained by rare events in biology (developmental defects), accident, culture (e.g. war), etc. This is not some kind of flaw in evolutionary theory, and it is pretty silly to argue otherwise.

  142. William J Murray

    I’m sure you’ll agree that what is being illustrated is a “real world biological entity”

    All I see is someone making a rather meaningless mathematical calculation and claiming because he got a big number for a result the object must be designed. Indeed, the term “Functionally Specific, Complex Organization and associated Information” seems to have been invented by kairosfocus and appears nowhere except on here UD, which should give you a good idea of its scientific worth.

    Sadly, kairosfocus makes the same dumb mistake that so many other ID proponents do: You can’t calculate the probability of a long term feedback process by just viewing the end result. You have to take into account the history of each step.

    Simple fact is, with iterative processes that retain filtered heritable variations it’s trivially easy to exceed the 500 – 1000 bit threshold claimed to indicate FSCO/I ‘design’. GAs do it all the time when they produce results that weren’t consciously designed. Dr. Dembski got rightly hammered on this when he first came out with his ‘Explanatory Filter’, which is a big part of why he abandoned the idea.

    As an aside, I’ve long since learned to skip over the posts of both kariosfocus and BA77. Both do nothing but repeat the same long-winded, pointless, droning screeds over and over and over. They’re a waste of bandwidth.

  143. GinoB:

    What is your point? Do you want to show that random variation exists? I think we all agree with that.

    The point is if RV can generate complex functional information. It can’t.

    The works you quote are fine. For me, they are as much ID works as they are darwinist works for you.

    A good work gives us facts. Facts are not labeled as “ID” or “darwinism”. It’s our duty to reason well on facts.

    By the way, thank you for quoting the Li paper. It is interesting indeed. Still vague, but I believe that is the right direction for research.

    Obviously, in no way it means what you seem to imply.

    Finallly, both kairosfocus and I have debated in detail the metric of dFSCI here. For an application to protein domains, please look at the Durston method and paper:

    http://www.ncbi.nlm.nih.gov/pm.....2-4-47.pdf

  144. Neither of those papers (as far as I can tell from the abstracts) move beyond the trivially accepted RM & NS capacity for successful microevolutionary variance within a current morphological framework of self-replicating and self-regulating populations.

    What “features” I am referring to are macroevolutionary features.

    The point of this thread isn’t a challenge that RM & NS do not exist, or do not produce some successful variance and distribute that variance throughout the species, but rather whether that process can be shown to be categorically sufficient to produce the macroevolutionary features necessary to move microbes to Mozart – such as, creating novel, functional biological mechanisms/features like a bacterial flagellum, stereoscopic vision or sexual reproduction.

    Until that process is demonstrated to be categorically sufficient, showing that it can generate minor variances within a species over the course of tens of thousands of generations only restates the already known and trivially accepted. Until demonstrated to be causally sufficient for the task proposed (as referred to in the title), it is a hasty generalization to believe that a process sufficient for accomplishing a minor variance is also sufficient for accomplishing any combination and accumulation of variances.

  145. GinoB,

    You said:

    You can’t calculate the probability of a long term feedback process by just viewing the end result. You have to take into account the history of each step.

    I have a few things to raise, if you don’t mind.

    1. No one disputes evolution is capable of adapting existing species. But evidence suggests it can’t do more than that. Evidence suggests that evolution is not powerful enough to produce new species.

    2. You doubted the validity of the metric. Well, suggest a similar metric or at least something measurable for the theory of evolution. We have at least something one can discuss and, if s/he wishes, dismiss on grounds of philosophical commitments. In the case of macroevolution we don’t have even that. The absense of a rigorous mathematical foundation underneath the TOE is recognised by evolutionists (a vacant position for a mathematician to attempt to start doing that was recently advertised at Oxford, UK, if I remember rightly). Because the evolutionists do not currently have such a solid foundation, they are unable to shut skeptics up once and for all. Do it, if you can.

    3. What is it that in your opinion greatly increases the odds of a success story for evolution, at one such step?

    4. Also, what you are apparently leaving out of the equation is that we can test this metric on human artefacts that we know have been designed and see if it works.

    5. What do you call long-term? I hope it is not absolute time but some normalised metric, something like the number of generations. Was anything like tissue/organ/body plan seen evolve say for fruit flies over a sufficient number of generations? Let’s take another vivid example, the Chernobyl nuclear power plant explosion in 1986. A lot of monstrosity came out as a result but none of it, to my limited knowledge, has been fixed in subsequent generations. There were 6 ft tall mashrooms, two-headed calves &c. but nothing apparently that would have made Charles Darwin happier. It seems like a big opportunity for biological novelty was lost.

  146. 146

    All I see is someone making a rather meaningless mathematical calculation and claiming because he got a big number for a result the object must be designed. Indeed, the term “Functionally Specific, Complex Organization and associated Information” seems to have been invented by kairosfocus and appears nowhere except on here UD, which should give you a good idea of its scientific worth.

    If the scientific worth of a proposed scientific commodity was calculated by its popular use, then we’d still be using 17th-century terms and concepts, as no new terms or concepts would have any “scientific worth”. The scientific worth of the concept of FSCI is regulated to it’s usefulness in rigorously distinguishing, predicting and retrodicting that which it is supposed to quantify. In the articles I directed you to, kairosfocus exhaustively shows the scientific history of both the concept and the applied terms to demonstrate that FSCO/I only refines long-used and applied scientific terms and concepts into a useful formulaic concept.

    Sadly, kairosfocus makes the same dumb mistake that so many other ID proponents do: You can’t calculate the probability of a long term feedback process by just viewing the end result. You have to take into account the history of each step.

    If you cannot calculate the probability that a feedback process can generate the end result it is proposed to have generated, then how can one claim with any significant value that it did so?

    Simple fact is, with iterative processes that retain filtered heritable variations it’s trivially easy to exceed the 500 – 1000 bit threshold claimed to indicate FSCO/I ‘design’.

    How is it that first you claim that the FSCO/I for design calculation is a “meaningless mathematical calculation” and imply it is of little or no scientific value, and then turn around and claim that it is a fact that “iterative processes that retain filtered heritable varations” can trivially exceed the proposed threshhold of ID? Where was this fact established in scientific literature if, as you say, the concept is only used here at UD?

    You can’t have it both ways; either the FSCO/I calculated threshold is a scientifically valid commodity that can be factually applied (whether to support or contra-indicate an ID conclusion), or it is not. You’ve just contradicted yourself.

    Please refer me to the papers where it has been shown that the process you describe has been shown to factually generate 1000+ bits of novel FSCO/I (which would, I imagine, be difficult, since you also say only UD uses that term/concept). Or is that a case you wish to make on your own here?

    GAs do it all the time when they produce results that weren’t consciously designed. Dr. Dembski got rightly hammered on this when he first came out with his ‘Explanatory Filter’, which is a big part of why he abandoned the idea.

    If the concept of FSCO/I was invented by kairosfocus and is only used here at UD and has little or no scientific value, how do you propose to substantiate your claim that genetic algorithms produce non-trivial amounts of FSCO/I?

    As an aside, I’ve long since learned to skip over the posts of both kariosfocus and BA77. Both do nothing but repeat the same long-winded, pointless, droning screeds over and over and over. They’re a waste of bandwidth.

    This comment, and your use of the pejorative term “dumb” above, IMO outs you as an insincere interlocutor on this topic. Those two contributors reiterate highly pertinent rebuttals and explanations where indicated because posters (like you) erect the same straw man and diversionary “arguments” over and over, whether willfully or ignorantly.

    Note how your argument above is self-contradictory. Either a metric exists that can validate RM & NS as sufficient to produce the features being challenged, or it does not. If it does not, it cannot be claimed that RM & NS are sufficient. That’s basic logic, no advanced degree required. You can’t have it both ways; you can’t say that no such metric exists in science, and then claim that the proposed process in fact generated the outcomes proposed to have been caused by the process.

    Also, either the FSCO/I metric is scientifically valid and can be factually measured (whether for or against an ID conclusion), or it is not and can not. You can’t have it both ways. It reminds me of when the mainstream scientific community was saying that ID couldn’t be falsified, and then wrote papers/books they claimed falsified it.

    You might try reading what BA77 and kairosfocus write, even though it takes a lot of effort and time, to really understand what they are explaining. A person who was sincerely trying to get to the truth of the matter about ID has no reason to resort to ad hominem.

  147. NickMatzke:

    Tell that to people who measure the level of drug resistance e.g. in malaria populations.

    Man are you dense. Sure we can tell which will live or die if we make that determination.

    There are many ways to legitimately infer the action of NS.

    Sure- let’s hear about them.

    One is watching it happen.

    Unfoirtunately for you when we do observe it happening it doesn’t support your position as all that comes from it is a wobbling stability- no long-term evolution.

    Another is looking at the genomes of populations of organisms for the signatures of selective sweeps.

    that would be subjective- as in saying “it must have been NS”.

    And, besides, you accept that NS exists and happens, so what the heck are you arguing about?

    It has never been observed to do what your position claims.


    Nature does not select and whatever works good enough survives and reproduces.

    Way to dance away from your original argument based on Larry Moran’s quote.

    That you think that is what happened tells me you are totally clueless.

    Natural selection is a minor player- and tere isn’t any selecting going on- all that still stands unrefuted.


    As for “strong selection”, well we see that when humans are involved, for example in infections when anti-biotics are used. The surviving bacteria are those with loss-of-function mutations which isn’t the type of change your position requires.

    This is only sometimes true, and often repaired by selection of additional compensatory mutations.

    Any examples of it not being true?

    As for name-calling- well Nick that is all you do so please put a sock in it.

  148. Eugene S

    Evidence suggests that evolution is not powerful enough to produce new species.

    Oh please, stop with the “if I ignore the evidence then the evidence doesn’t exist!” schtick. There are literally thousands of colleges, universities, natural history museums, and millions of pages of on-line text where you can learn about the evidence for speciation.

    The absense of a rigorous mathematical foundation underneath the TOE is recognised by evolutionists

    There is a whole branch of science, Population Genetics, that deals with mathematical evolutionary metrics.

    Also, what you are apparently leaving out of the equation is that we can test this metric on human artefacts that we know have been designed and see if it works.

    The way archaeologists determine if a find is human produced (say a primitive stone ax) or just a natural rock is by comparing the object with other known human designed similar objects. Not superficial similarities, not analogies (like flagella and outboard motors) but actual known designed objects. They don’t just look at the rock itself but look for other signs of manufacture, things like specific chipping patterns, flint flakes, a work area where the tool was produced, and the source of the material. They also go to great lengths to identify the likely designer - who was living in the area at the time, what was their level of technology at the time, etc.

    The whole ID party line “it’s not about the designer, just the design” is one of the most intellectually vacuous bits of nonsense that’s ever come down the pike.

    What do you call long-term?

    Life has been on this planet and evolving for over 3 billion years. Multi-cellular life has been around and reproducing for at least the last 650 million years. That seems pretty long term to me.

  149. Meleagar

    Neither of those papers (as far as I can tell from the abstracts) move beyond the trivially accepted RM & NS capacity for successful microevolutionary variance within a current morphological framework of self-replicating and self-regulating populations.

    What “features” I am referring to are macroevolutionary features.

    The point of this thread isn’t a challenge that RM & NS do not exist, or do not produce some successful variance and distribute that variance throughout the species, but rather whether that process can be shown to be categorically sufficient to produce the macroevolutionary features necessary to move microbes to Mozart

    Please explain the barrier mechanism that prevents microevolutionary changes from accumulating over time into macroevolutionary ones.

    What would stop a terrestrial mammal’s paw from evolving into an aquatic mammal’s flipper given sufficient time? Saying “we’ve never seen it happen” isn’t an answer as the process takes way too long to see in real time. No one’s ever seen a whole mountain rise in real time from the collision of tectonic plates, but no one claims our understanding of mountain formation is wrong.

    We can see micro-E in real time, and we have plenty of evidence micro-E changes can and have accumulated over time. Do you have any evidence that they can’t?

  150. GB,

    Nice try. Not solid enough, unfortunately. These metrics are not sufficient to prove macroevolution is a fact. Population genetics has not tunred macroevolution from a hypothesis to scientifically established truth.

    I repeat my question. What is it that you believe is able to considerably affect the likelihood of generating a large quanitity of information spontaneously at a single evolutionary step?

  151. 151

    Please explain the barrier mechanism that prevents microevolutionary changes from accumulating over time into macroevolutionary ones.

    I didn’t claim there was a barrier mechanism. I challenged those who claim the process is sufficient for causal explanation to provide the metric that demonstrates their proposed process to be categorically capable of so doing. The onus is on the claimant, not on the challenger, to provide sufficient warrant for their claim.

    What would stop a terrestrial mammal’s paw from evolving into an aquatic mammal’s flipper given sufficient time? Saying “we’ve never seen it happen” isn’t an answer as the process takes way too long to see in real time. No one’s ever seen a whole mountain rise in real time from the collision of tectonic plates, but no one claims our understanding of mountain formation is wrong.

    I didn’t claim anything prevented it, or that it doesn’t happen. I’ve challenged you (and anyone else so willing) to adequately support your claim that the process you describe is categorically capable of producing the features it is claimed to produce.

    One might claim that the collision of tectonic plates produces all sorts of surface features; but because that process can be shown (categorically) to be able to produce some surface features doesn’t mean it is safe to assume it can produce **all** surface features. That’s called a hasty generalization and is a logical error.

    We can see micro-E in real time, and we have plenty of evidence micro-E changes can and have accumulated over time. Do you have any evidence that they can’t?

    I am under no obligation to produce such evidence since I haven’t claimed that microevolutionary changes do not occur or do not accumulate. It seems you are attempting to shift the burden.

    Either you can provide the metric that RM & NS is categorically sufficient to explain the features in question, or you are just assuming that accumlations of small variations can lead to the generation of novel, functioning macroevolutionary features, which is a hasty generalization.

  152. “Please explain the barrier mechanism that prevents microevolutionary changes from accumulating over time into macroevolutionary ones.”

    Biological systems are necessarily highly complex and fine-tuned. So it is the fine-tuning and minimal function. Taking life in all its entirety, even climbing the mount improbable from behind is not sufficient to completely dismiss the complexity argument, because in this case we still rely on multiple coincidences and wishful thinking. The archetypal example of the mousetrap illustrates that for a trait to be exapted there has to be some initial functionality present. Gene duplication and recombination cannot be responsible for all diversity of life because the whole is not necessarily equal to the sum of its parts. Biology cannot be reduced to physics and chemistry.

  153. If I may add a bit to illustrate just how far off base neo-Darwinists are with their extrapolation of micro-evolutionary variations to explain the origination of all life on earth;,,,, Besides the fact that all micro-evolutionary (sub-speciation) events, away from a parent species, are shown to lose information (Behe, Sanford, Spetner, etc.. etc..), the primary reason why micro-evolutionary events will not accumulate over time is because of what is termed the ‘poly-constraint’ on a genome. Poly-constraint on a genome is what is wrought on the genome by the extreme poly-functionality of the genome:

    notes:

    Poly-Functional Complexity equals Poly-Constrained Complexity

    The primary problem that poly-functional complexity presents for neo-Darwinism, or even Theistic Evolutionists is this:

    To put it plainly, the finding of a severely poly-functional/polyconstrained genome by the ENCODE study has put the odds, of what was already astronomically impossible, to what can only be termed fantastically astronomically impossible. To illustrate the monumental brick wall any evolutionary scenario (no matter what “fitness landscape”) must face when I say genomes are poly-constrained to random mutations by poly-functionality, I will use a puzzle:

    If we were to actually get a proper “beneficial mutation’ in a polyfunctional genome of say 500 interdependent genes, then instead of the infamous “Methinks it is like a weasel” single element of functional information that Darwinists pretend they are facing in any evolutionary search, with their falsified genetic reductionism scenario I might add, we would actually be encountering something more akin to this illustration found on page 141 of Genetic Entropy by Dr. Sanford.

    S A T O R
    A R E P O
    T E N E T
    O P E R A
    R O T A S

    Which is translated ;
    THE SOWER NAMED AREPO HOLDS THE WORKING OF THE WHEELS.

    This ancient puzzle, which dates back to 79 AD, reads the same four different ways, Thus, If we change (mutate) any letter we may get a new meaning for a single reading read any one way, as in Dawkins weasel program, but we will consistently destroy the other 3 readings of the message with the new mutation.

    This is what is meant when it is said a poly-functional genome is poly-constrained to any random mutations.

    The puzzle I listed is only poly-functional to 4 elements/25 letters of interdependent complexity, the minimum genome is poly-constrained to approximately 500 elements (genes) at minimum approximation of polyfunctionality. For Darwinist to continue to believe in random mutations to generate the staggering level of complexity we find in life is absurd in the highest order!

    Further notes:

    “Whatever we may try to do within a given species, we soon reach limits which we cannot break through. A wall exists on every side of each species. That wall is the DNA coding, which permits wide variety within it (within the gene pool, or the genotype of a species)-but no exit through that wall. Darwin’s gradualism is bounded by internal constraints, beyond which selection is useless.”
    R. Milner, Encyclopedia of Evolution (1990)

    Unexpectedly small effects of mutations in bacteria bring new perspectives – November 2010
    Excerpt:,,, using extremely sensitive growth measurements, doctoral candidate Peter Lind showed that most mutations reduced the rate of growth of bacteria by only 0.500 percent. No mutations completely disabled the function of the proteins, and very few had no impact at all. Even more surprising was the fact that mutations that do not change the protein sequence had negative effects similar to those of mutations that led to substitution of amino acids. A possible explanation is that most mutations may have their negative effect by altering mRNA structure, not proteins, as is commonly assumed.
    http://www.physorg.com/news/20.....teria.html

    Mutations : when benefits level off – June 2011 – (Lenski’s e-coli after 50,000 generations;,, approx. equal to 1,000,000 years of human evolution)
    Excerpt: After having identified the first five beneficial mutations combined successively and spontaneously in the bacterial population, the scientists generated, from the ancestral bacterial strain, 32 mutant strains exhibiting all of the possible combinations of each of these five mutations. They then noted that the benefit linked to the simultaneous presence of five mutations was less than the sum of the individual benefits conferred by each mutation individually.
    http://www2.cnrs.fr/en/1867.htm?theme1=7

    Notes on the extreme level of poly-functionality being dealt with:

    Scientists Map All Mammalian Gene Interactions – August 2010
    Excerpt: Mammals, including humans, have roughly 20,000 different genes.,,, They found a network of more than 7 million interactions encompassing essentially every one of the genes in the mammalian genome.
    http://www.sciencedaily.com/re.....142044.htm

    Insight into cells could lead to new approach to medicines
    Excerpt: Scientists expected to find simple links between individual proteins but were surprised to find that proteins were inter-connected in a complex web. Dr Victor Neduva, of the University of Edinburgh, who took part in the study, said: “Our studies have revealed an intricate network of proteins within cells that is much more complex than we previously thought.

    Three Subsets of Sequence Complexity and Their Relevance to Biopolymeric Information – David L. Abel and Jack T. Trevors – Theoretical Biology & Medical Modelling, Vol. 2, 11 August 2005, page 8
    “No man-made program comes close to the technical brilliance of even Mycoplasmal genetic algorithms. Mycoplasmas are the simplest known organism with the smallest known genome, to date. How was its genome and other living organisms’ genomes programmed?”
    http://www.biomedcentral.com/c.....2-2-29.pdf

    Simplest Microbes More Complex than Thought – Dec. 2009
    Excerpt: PhysOrg reported that a species of Mycoplasma,, “The bacteria appeared to be assembled in a far more complex way than had been thought.” Many molecules were found to have multiple functions: for instance, some enzymes could catalyze unrelated reactions, and some proteins were involved in multiple protein complexes.”

    First-Ever Blueprint of ‘Minimal Cell’ Is More Complex Than Expected – Nov. 2009
    Excerpt: A network of research groups,, approached the bacterium at three different levels. One team of scientists described M. pneumoniae’s transcriptome, identifying all the RNA molecules, or transcripts, produced from its DNA, under various environmental conditions. Another defined all the metabolic reactions that occurred in it, collectively known as its metabolome, under the same conditions. A third team identified every multi-protein complex the bacterium produced, thus characterising its proteome organisation.
    “At all three levels, we found M. pneumoniae was more complex than we expected,”
    http://www.sciencedaily.com/re.....173027.htm

    3-D Structure Of Human Genome: Fractal Globule Architecture Packs Two Meters Of DNA Into Each Cell – Oct. 2009
    Excerpt: the information density in the nucleus is trillions of times higher than on a computer chip — while avoiding the knots and tangles that might interfere with the cell’s ability to read its own genome. Moreover, the DNA can easily unfold and refold during gene activation, gene repression, and cell replication.
    http://www.sciencedaily.com/re.....142957.htm

    “In the last ten years, at least 20 different natural information codes were discovered in life, each operating to arbitrary conventions (not determined by law or physicality). Examples include protein address codes [Ber08B], acetylation codes [Kni06], RNA codes [Fai07], metabolic codes [Bru07], cytoskeleton codes [Gim08], histone codes [Jen01], and alternative splicing codes [Bar10].
    Donald E. Johnson – Programming of Life – pg.51 – 2010

    DNA Caught Rock ‘N Rollin’: On Rare Occasions DNA Dances Itself Into a Different Shape – January 2011
    Excerpt: Because critical interactions between DNA and proteins are thought to be directed by both the sequence of bases and the flexing of the molecule, these excited states represent a whole new level of information contained in the genetic code,
    http://www.sciencedaily.com/re.....104244.htm

    Systems biology: Untangling the protein web – July 2009
    Excerpt: Vidal thinks that technological improvements — especially in nanotechnology, to generate more data, and microscopy, to explore interaction inside cells, along with increased computer power — are required to push systems biology forward. “Combine all this and you can start to think that maybe some of the information flow can be captured,” he says. But when it comes to figuring out the best way to explore information flow in cells, Tyers jokes that it is like comparing different degrees of infinity. “The interesting point coming out of all these studies is how complex these systems are — the different feedback loops and how they cross-regulate each other and adapt to perturbations are only just becoming apparent,” he says. “The simple pathway models are a gross oversimplification of what is actually happening.”
    http://www.nature.com/nature/j.....0415a.html

    “Today there is an explosion of knowledge going on in the study of gene regulatory networks. But it is not led, assisted, or even inspired by the theory of evolution. “We have little empirical knowledge on the evolutionary history of such networks.”– Dean, Antony M., Joseph W. Thornton. September 2007. Mechanistic approaches to the study of evolution: the functional synthesis. Nature Reviews Genetics, Vol. 8, pp. 675-688.

    Music:

    MercyMe – Beautiful
    http://www.youtube.com/watch?v=1vh7-RSPuAA

  154. GB,

    Can I ask you a question? Is there anything at all the TOE can definitely say is impossible? Please illustrate with concrete examples if you can.

  155. 155

    There are literally thousands of colleges, universities, natural history museums, and millions of pages of on-line text where you can learn about the evidence for speciation.

    Evidence that species diverged is not evidence that a proposed process is a sufficient explanation for that divergence.

    There is a whole branch of science, Population Genetics, that deals with mathematical evolutionary metrics.

    The distribution of acquired traits in a population is not being debated to my knowledge.

    The way archaeologists determine if a find is human produced (say a primitive stone ax) or just a natural rock is by comparing the object with other known human designed similar objects. Not superficial similarities, not analogies (like flagella and outboard motors) but actual known designed objects. They don’t just look at the rock itself but look for other signs of manufacture, things like specific chipping patterns, flint flakes, a work area where the tool was produced, and the source of the material. They also go to great lengths to identify the likely designer – who was living in the area at the time, what was their level of technology at the time, etc.

    You’ve some very big begged questions: what are the initial reasonable grounds for suspecting an object might be designed before one gets to any further analysis?

    Second: Is there any logical reason to assume that humans are the only entities in the universe that produce intelligently designed artifacts? Or ever have? If we assume that humans are potentially not the only intelligent designers in the universe, how would we recognize non-human, intelligently-designed artifacts if not by (1) excluding them as being sufficiently explained by non-intelligent natural forces, and (2) comparing them favorably to the only other example of ID we have – human ID?

    The whole ID party line “it’s not about the designer, just the design” is one of the most intellectually vacuous bits of nonsense that’s ever come down the pike.

    That doesn’t change the fact that one must first identify that an object was intelligently designed before one can make any headay whatsoever on the nature of the designer.

    Life has been on this planet and evolving for over 3 billion years. Multi-cellular life has been around and reproducing for at least the last 650 million years. That seems pretty long term to me.

    Without a metric that can scientifically quantify how much time is necessary for the proposed process to acquire the kinds of features in question, one has no idea if 3-4 billion years is more than enough, just enough, or not nearly enough time, so one has no basis by which to claim it is a long enough time.

  156. William J Murray

    GinoB: “Please explain the barrier mechanism that prevents microevolutionary changes from accumulating over time into macroevolutionary ones.”

    I didn’t claim there was a barrier mechanism.

    I didn’t say you did. That was a request to Meleagar, who did make such a claim.

    I challenged those who claim the process is sufficient for causal explanation to provide the metric that demonstrates their proposed process to be categorically capable of so doing. The onus is on the claimant, not on the challenger, to provide sufficient warrant for their claim.

    Why in the world do you think we have to have a mathematical metric to determine the cause of historical events? What is the metric that lets us determine the cause of WW2? What is the metric that lets us determine the cause for the dinosaurs’ extinction?

    We determine the cause of historical events by examining the evidence the events left behind. As for evolutionary processes being sufficient, this has been demonstrated to the satisfaction of the scientific community for over 100 years. There are literally thousands of colleges, universities, natural history museums, and millions of pages of on-line text where you can learn about the evidence. People spend their whole lives studying and getting PhDs and only touch on a tiny portion of it. There’s far too much of it to give it adequate coverage here on this tiny blog. Get thee to a library!

    If the concept of FSCO/I was invented by kairosfocus and is only used here at UD and has little or no scientific value, how do you propose to substantiate your claim that genetic algorithms produce non-trivial amounts of FSCO/I?

    FSCO/I is just another failed attempt to add legitimacy to personal incredulity, i.e “it’s sooooo complex, it must be designed!!”. The terms are so vaguely defined as to be meaningless (what does functional mean? what does complex organization mean?), and the logic is flawed from the get go by the false assumption “all complex things are designed”.

    As an easy example, here’s an online fractal generator. You give it the starting points and a few simple rules, and the feedback process will produce amazingly complex designs (Mandelbrot sets, Julia sets, etc.) that have millions of bits of ‘FSCO/I’. The patterns are ‘organized’, and ‘functional’ – they function as artwork on my computer desktop.

    ID is going to keep getting nowhere as long as all it does is attack evolutionary theory instead of providing its own positive evidence.

  157. Can I ask you a question? Is there anything at all the TOE can definitely say is impossible? Please illustrate with concrete examples if you can.

    Yes. A centaur. Or any chimera, once hybridisation has ceased to be physically possible.

    Also evolution back up the way it came down. Marine mammals are very different from fish, even though they live in a similar environment. A whale with fish-gills would be virtually impossible, although gill-like structures might well evolve from some mammalian feature.

  158. psst, Gino: Meleager and William Murray are the same person :)

  159. gpuccio

    GinoB:

    What is your point? Do you want to show that random variation exists? I think we all agree with that.

    The point is if RV can generate complex functional information. It can’t.

    Since no one in the scientific community says or thinks just RV by itself creates biological complexity, what’s your point?

  160. 160

    Yeah, sometimes I log in under the old name. Sorry about the confusion.

  161. William J Murray

    That doesn’t change the fact that one must first identify that an object was intelligently designed before one can make any headay whatsoever on the nature of the designer.

    The first step in identifying suspected design, and the most important step, is understanding the identity and capabilities of the designer. That’s the big part IDists won’t own up to, because they know their Omnipotent God wouldn’t be allowed in science classes. So they keep playing the “it’s not about the designer” game, and science keeps just rolling its eyes.

    Without a metric that can scientifically quantify how much time is necessary for the proposed process to acquire the kinds of features in question, one has no idea if 3-4 billion years is more than enough, just enough, or not nearly enough time, so one has no basis by which to claim it is a long enough time.

    We do have metrics in the form of the fossil / geologic record. For example, we have whole museums full of evidence that observed evolutionary processes did indeed do the job of changing terrestrial mammals into aquatic cetaceans in an approximately 60 MY time span. Your demand for a more detailed rate of change metric (which would be different in every case BTW) doesn’t negate the existing evidence one iota.

  162. OK, no worries. I’ll keep that in mind.

    I’ll also do my best to keep things civil. I appreciate that you’ve been doing so too.

  163. GinoB:

    The whole ID party line “it’s not about the designer, just the design” is one of the most intellectually vacuous bits of nonsense that’s ever come down the pike.

    Umm REALITY dictates that in the absence of direct observation the only possible way to make any scientific determination about the designer(s) or the specific process(es) used is by studying the design in question.

    THAT is how it is done in archaeology and forensic science.

    The point being is we don’t have to know anything about the designer nor the processes used BEFORE we can determine design is present.

    The first step in identifying suspected design, and the most important step, is understanding the identity and capabilities of the designer.

    And who are YOU to make such a claim?

    Heck we understand the capabilities by studying the design! How do we know stone age people were capable of building Stonehenge? STONEHENGE!

    How do we know bronze age people were capable of creating the antikythera mechanism? The antikythera mechanism!

    And science cares about REALITY- it does NOT care if God is part of that reality. There isn’t any separation of church and state in science.

  164. “Yes. A centaur. Or any chimera, once hybridisation has ceased to be physically possible.”

    Prove it by means of the TOE.

    What exactly determines physical impossibility of such hybridisation, from the point of view of the TOE?

    What exactly precludes centaurs from existing by the TOE? They are indeed clever, strong, quick animals that are better adapted to the environment than either horses or humans.

    A pegasus is more clever and faster than birds and positively better adapted than horses because it can fly as fast as it can run. Why is it impossible for pegassus to exist?

  165. GinoB:

    FSCO/I is just another failed attempt to add legitimacy to personal incredulity, i.e “it’s sooooo complex, it must be designed!!”.

    Umm the design inference requires more than mere complexity.

    The terms are so vaguely defined as to be meaningless (what does functional mean? what does complex organization mean?), and the logic is flawed from the get go by the false assumption “all complex things are designed”.

    1- That ain’t the assumption

    2- our whole position is vaguely defined

    3- What does “functional” mean? Is THAT your argument?

    Your criticisms are hollow because all you have to do is step up and start producing positive evidence in support of your position and ID would go away. But you can’t so all you have is to attack ID with your nonsense.

  166. 1- That ain’t the assumption

    2- Your whole position is vaguely defined

    3- What does “functional” mean? Is THAT your argument?

  167. Gino, as to this one deception out of many:

    We do have metrics in the form of the fossil / geologic record. For example, we have whole museums full of evidence that observed evolutionary processes did indeed do the job of changing terrestrial mammals into aquatic cetaceans in an approximately 60 MY time span.

    Yet what you say is not true, and is fact a blatant deception, whether you are aware of it or not:

    Whale Evolution vs. The Actual Fossil Evidence
    http://vimeo.com/30921402

    further notes;

    Whale Evolution Vs. Population Genetics – Richard Sternberg PhD. in Evolutionary Biology – video
    http://www.metacafe.com/watch/4165203

    A Whale of a Problem for Evolution: Ancient Whale Jawbone Found in Antartica – JonathanM – October 2011
    Excerpt: Argentine paleontologist Marcelo Reguero said the fossilized archaeocete jawbone found in February dates back 49 million years. In evolutionary terms, that’s not far off from the fossils of even older proto-whales from 53 million years ago that have been found,,,
    http://www.uncommondescent.com.....antartica/

    This following is humorous as to what the presumed ‘vestigial legs’ of the whale actually turned out to be:

    An Email Exchange Regarding “Vestigial Legs” Pelvic Bones in Whales by Jim Pamplin
    Excerpt: The pelvic bones (supposed Vestigial Legs) of whales serve as attachments for the musculature associated with the penis in males and its homologue, the clitoris, in females. The muscle involved is known as the ischiocavernosus and is quite a powerful muscle in males. It serves as a retractor muscle for the penis in copulation and probably provides the base for lateral movements of the penis. The mechanisms of penile motion are not well understood in whales. The penis seems to be capable of a lot of independent motion, much like the trunk of an elephant. How much of this is mediated by the ischiocavernosus is not known.
    In females the anatomical parts are smaller and more diffuse. I would imagine that there is something homologous to the perineal muscles in man and tetrapods, which affect the entire pelvic area – the clitoris, vagina and anus.
    The pelvic rudiments also serve as origins for the ischiocaudalis muscle, which is a ventral muscle that inserts on the tips of the chevron bones of the spinal column and acts to flex the tail in normal locomotion.
    http://www.darwinisdead.com/an.....arding.htm

  168. Well natural selection has never been observed to create anything except for a wobbling stability

  169. 169

    I didn’t say you did. That was a request to Meleagar, who did make such a claim.

    Sorry about the confusion – I am Meleagar. Sometimes I mistakenly log in under my old name. Please show me where I made such a claim under either name.

    Why in the world do you think we have to have a mathematical metric to determine the cause of historical events? What is the metric that lets us determine the cause of WW2? What is the metric that lets us determine the cause for the dinosaurs’ extinction?

    You are making a categorical error here. Because I am asking for a metric to support the contention that a proposed process is a sufficient explanation for what it claims to explain, and that process happens to be largely historical (but still in operation), doesn’t mean that I believe **all** historical claims require a supportive metric.

    The reason a supportive metric is required for the particular claim that RM & NS is categorically capable of producing the features it is claimed to have produced is because RM and NS as an explanatory process through history is only describable in stochastic terms; there’s no other way to vet RM & NS as sufficiently capable of causing the proposed effects.

    Unless you’d like to propose some other method of vetting them as categorically sufficient?

  170. “all complex things are designed”

    Oh boy, that is simply wrong. You have the wrong idea of ID. Before criticising, it is advisable to familiarise yourself with the basics about what you are criticising. Otherwise, your credit score as a debater goes down.

    There is a conceptual difference between complexity and biological function. E.g. a random string of AAs can be complex in the sense of Kolmogorov (i.e. non-compressible) but non-functional.

  171. Gino you sure talk a big game here:

    There are literally thousands of colleges, universities, natural history museums, and millions of pages of on-line text where you can learn about the evidence. People spend their whole lives studying and getting PhDs and only touch on a tiny portion of it. There’s far too much of it to give it adequate coverage here on this tiny blog. Get thee to a library!

    Perhaps, out of those, literally thousands of colleges, universities, natural history museums, and millions of pages of on-line text, you can let us know just a few of the specific studies that Dr. Michael Behe overlooked in this summary paper of 4 decades of lab work:

    “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain – Michael Behe – December 2010
    Excerpt: In its most recent issue The Quarterly Review of Biology has published a review by myself of laboratory evolution experiments of microbes going back four decades.,,, The gist of the paper is that so far the overwhelming number of adaptive (that is, helpful) mutations seen in laboratory evolution experiments are either loss or modification of function. Of course we had already known that the great majority of mutations that have a visible effect on an organism are deleterious. Now, surprisingly, it seems that even the great majority of helpful mutations degrade the genome to a greater or lesser extent.,,, I dub it “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain.(that is a net ‘fitness gain’ within a ‘stressed’ environment i.e. remove the stress from the environment and the parent strain is always more ‘fit’)
    http://behe.uncommondescent.co.....evolution/

    Michael Behe talks about the preceding paper on this podcast:

    Michael Behe: Challenging Darwin, One Peer-Reviewed Paper at a Time – December 2010
    http://intelligentdesign.podom.....3_46-08_00

  172. GinoB:

    Since no one in the scientific community says or thinks just RV by itself creates biological complexity, what’s your point?

    Well, you quoted two papers showing trivial examples of simple random variation, and I just wondered why.

    Of course I am well aware that according to the neodarwinian model RV is “helped” by NS. I have discussed that many times, even recently.

    My general point is simple:

    a) RV cannot generate dFSCI

    b) RV + NS in principle could, but only if the pathway to the complex information could be deconstructed into steps of low enough functional complexity, each of them naturally selectable (that is, bearing a definite reproductive advantage).

    Point b) is not true. Not only it is not true in the general case (which should be the true requirement). It is not true in any known case for any basic protein domain.

    It’s as simple as that.

  173. 173

    The first step in identifying suspected design, and the most important step, is understanding the identity and capabilities of the designer.

    How does one say anything about the identity or capability of a designer before they even have an item they suspect of being designed?

    That’s the big part IDists won’t own up to, because they know their Omnipotent God wouldn’t be allowed in science classes. So they keep playing the “it’s not about the designer” game, and science keeps just rolling its eyes.

    An appeal to motivation is irrelevant to the debate at hand. You might make room in your conception of the ID community that not everyone has such ulterior motives and focus on the facts and logic of the arguments presented.

    We do have metrics in the form of the fossil / geologic record. For example, we have whole museums full of evidence that observed evolutionary processes did indeed do the job of changing terrestrial mammals into aquatic cetaceans in an approximately 60 MY time span. Your demand for a more detailed rate of change metric (which would be different in every case BTW) doesn’t negate the existing evidence one iota.

    You are making another categorical error here. The fossilized timeline evidence of descent has nothing whatsoever to contribute to the debate about whether or not RM & NS is a sufficient process to explain the features exhibited by those fossils except to provide a limitation of time in which RM & NS can achieve what they are claimed to have produced.

    One must show that RM & NS is a sufficient explanatory process that can get the job done within the timeframe indicated by the fossilized evidence; if the (as yet unprovided) RM & NS metric shows that the time frame is sufficient, then the timeframe becomes evidence in favor of RM & NS as sufficiently explanatory.

    Without the metric, though, we don’t know if the fossilized descent timeframe is evidence for or against RM & NS as a sufficient explanation.

    Another way of stating this is to ask: Is 10 years too little time to move microbe to Mozart? Is 100 years too little? Is one million years too little? A hundred million? A billion? Ten billion? 100 billion?

    How can one say, one way or another, with any confidence, until we have a categorically predictive (& retrodictive) metric that describes what RM & NS is and is not capable of producing (in general terms) given X resources and Y time (generations of reproduction), as it relates to the actual biological features that currently exist and historically existed as indicated by the fossil record?

    Faith that RM & NS could have produced what it is claimed to have produced in the time-frame allotted because 3-4 billion years “seems long enough” is not a rigorous, scientific support of the claim.

  174. GinoB:

    Anyway, in case you are interested in some further detail about my position, please look at my posts to Elizabeth (from #5 to #11) in this same thread.

    There you will find a rather detailed argumentation about the role of NS in the neodarwinian algorithm (and some other points).

  175. If pianos evolved in the stringed instrument category, why is it unacceptable for people to have evolved in the homo genus?

  176. 176
    material.infantacy

    “But in one of those two cases there is an absurdity of an infinite regress of causes …”

    Monotheism suggests that the first cause is personal, immaterial, and eternal.

    What is the material first cause, and what attributes does it possess?

    It can’t be personal, because then it would be God. It can’t be immaterial, because then it couldn’t be a material first cause. It can’t be eternal and impersonal, otherwise it would operate out of necessity, and the universe we inhabit would be long dead — and if it possessed a mechanistic attribute for generating universes eternally, then it would presuppose time, space, and physics, and would no longer qualify as a first cause; it would trigger an infinite regress.

  177. gpuccio

    GinoB: Since no one in the scientific community says or thinks just RV by itself creates biological complexity, what’s your point?

    Well, you quoted two papers showing trivial examples of simple random variation, and I just wondered why.

    That’s not what the papers showed. They showed the effects on fitness of variations and showed the effects to be independent of ‘need’.

    Of course I am well aware that according to the neodarwinian model RV is “helped” by NS. I have discussed that many times, even recently.

    You have also demonstrated that you still don’t understand it.

    My general point is simple:

    a) RV cannot generate dFSCI

    No one says it does, especially since your ‘dFSCI’ metric is a worthless made-up buzzterm not recognized by or used in the actual scientific community.

    b) RV + NS in principle could, but only if the pathway to the complex information could be deconstructed into steps of low enough functional complexity, each of them naturally selectable (that is, bearing a definite reproductive advantage).

    Point b) is not true.

    Your Point b) strawman is definitely not true, because there’s no requirement in evolution for every mutation to be positively selectable at every step. It is well documented that neutral mutations can and do accumulate in a population through drift, then combine with other later mutations to provide a reproductive benefit.

    You are attacking a worthless strawman version of the actual scientific theory, which is a major reason no one in the scientific community takes these claims seriously. It’s as simple as that.

  178. Point b) is not true. Not only it is not true in the general case (which should be the true requirement). It is not true in any known case for any basic protein domain.

    And you know this because you know the detailed history of the origin of protein domains?

  179. Joseph

    Well natural selection has never been observed to create anything except for a wobbling stability

    RV by itself doesn’t create new features or complexity.

    NS by itself doesn’t create new features or complexity.

    But the combined iterative process of RV filtered by NS with entities that retain heritable variations can and does easily create new features and complexity.

    You’ve only had that explained to you several dozen times by now.

  180. William J Murray

    How can one say, one way or another, with any confidence, until we have a categorically predictive (& retrodictive) metric that describes what RM & NS is and is not capable of producing (in general terms) given X resources and Y time (generations of reproduction), as it relates to the actual biological features that currently exist and historically existed as indicated by the fossil record?

    You can type that as many times as you like if it makes you feel better but it still won’t erase the existing evidence one tiny bit. We know from genetic studies and evo-devo studies of things like Hox genes that major morphological changes can happen quite rapidly compared to geological time, often in tens to hundreds of generations. We also have estimated mutational rates per generation for many extant species. There is no question in the scientific community that the observed processes are both capable and responsible for the evolutionary changes seen in the observed time frame.

    Your demand that we reject the evolutionary evidence unless you are given specific mathematical metrics is like claiming Hannibal never crossed the alps because we don’t have specific metrics on how fast and how far elephants can climb mountains.

  181. Joseph,
    What have you ever observed “the designer” creating?

    gpuccio,

    There you will find a rather detailed argumentation about the role of NS in the neodarwinian algorithm (and some other points).

    Have you ever thought about writing your observations up and submitting a paper based on them? If your argument holds water why not?

  182. 182

    You can type that as many times as you like if it makes you feel better but it still won’t erase the existing evidence one tiny bit.

    I haven’t attempted to erase any evidence; all I’ve done is ask for it to be presented, and have rightfully pointed out that the evidence you have referred to – such as the timeline of the fossil evidence – cannot support the your contention of RM & NS sufficiency without a metric that shows the time available to be sufficient for the process to achieve the results in question.

    We know from genetic studies and evo-devo studies of things like Hox genes that major morphological changes can happen quite rapidly compared to geological time, often in tens to hundreds of generations. We also have estimated mutational rates per generation for many extant species.

    Then it should be no problem to use that information to form the basis of a substantive predictive/retrodictive metric that describes the minimum time/reproductive resources necessary to acquire Mozart from a microbe via RM & NS in light of such known rates. Please direct me to the work that provides this analysis.

    There is no question in the scientific community that the observed processes are both capable and responsible for the evolutionary changes seen in the observed time frame.

    So the scientists that signed the “Dissent from Darwinism” document at http://www.dissentfromdarwin.org, which states:

    “We are skeptical of claims for the ability of random mutation and natural selection to account for the complexity of life. Careful examination of the evidence for Darwinian theory should be encouraged.”

    are not part of the scientific community?

    Whether or not there is “any question” in the scientific community “that the observed processes are both capable and responsible for the evolutionary changes seen in the observed time frame” is irrelevant to the challenge at hand; that the process be shown to be so capable via a scientific metric that can vet it in terms of adequate time and reproductive resources.

    Without such a qualifying metric, what “the scientific community” believes or accepts as true is unsupportable. A claim isn’t made true just because there is scientific consensus.

    Your demand that we reject the evolutionary evidence unless you are given specific mathematical metrics is like claiming Hannibal never crossed the alps because we don’t have specific metrics on how fast and how far elephants can climb mountains.

    I haven’t asked anyone to reject anything, much less “demanded” it, and I haven’t claimed that RM & NS didn’t produce what what they are claimed to have produced; I have challenged you to support your assertion that it is a sufficient explanation.

    If you make the claim that Hannibal crossed the alps on elephants in X number of years, and I – being skeptical of such claims – challenge you to show that it is even theoretically possible, then you could easily support your claim by factoring in top land speed of elephants, distance, and time available, thus devising a verifying or falsifying metric.

    And that’s all I’m asking for: not proof that RM & NS did in fact make the trip; only that they are theoretically (categorically) capable of making the trip.

  183. 183

    By “capable of making the trip” – I mean, to cover the proposed distance on elephants in the amount of time asserted”.

    IOW, I’m not challenging that the trip was made, or that it occurred in the time allotted, but only that elephants are theoretically capable of covering that distance in that amount of time – meaning, I’m mot challenging common descent from microbe to mozart in the time allotted; I’m challenging that your “elephant” is capable of making that trip in the time allowed.

  184. Are you serious?

    A centaur is a chimera, that is, it has the torso of a human and the body, i.e. the four legs of a horse.

    That means it’s not a tetrapod, yet it has features from two separate tetrapod lineages.

    How could the ToE possibly account for such an animal, if it were found?

    I’m not saying that a centaur couldn’t have evolved – lots of things could have evolved but didn’t. But once a lineage has started, it can’t go back up the same trail (if this isn’t obvious to you, I guess I’ll try and explain, but I’m assuming you must have misunderstood my point)

    So if we found a fossil centaur, the ToE would pretty well have to be abandoned. It could not possibly explain how a creature that must belong to a hexapod lineage that left the vertebrates at a different point to the tetrapods could end up consisting of two different tetrapods.

  185. OK, fair enough, gpuccio, I shot from the hip. My bad. And I’m not sure I have time to address all your points now.

    If you want to catch up with me, try me at The Skeptical Zone.

    You’d be very welcome :)

  186. Elizabeth:

    Thanks for the invitation. Maybe I will. Other times I have debated in forums “on the other side”, but it is usually very tiring. At present, it is already difficult for me to find time to post at UD!

  187. Elizabeth:

    Are you sure you are not underestimating the darwinists’ creativity?

  188. I agree, but I don’t see the misleading potential. Of course I agree that the word “selection” is not a good one, but it is the one currently used (and not certainly created by us IDists).

    In practice most variants are near-neutral in effect on reproductive success, and so the chances of any new variant propagating through the population is heavily dependent on luck.

    Yes indeed, but that doesn’t that quite a lot won’t propagate and many do. That’s why I keep saying that the gene pool is constantly being drip-fed by near-neutral variants. This means that when any environmental change comes along, the population is excellently placed to adapt, as we see in what you would call “micro-evolution”. But there is no reason why that process can’t continue in one direction, rather than oscillate around a mean, as long as the drip-feed of new variants is fast enough to keep up with the environmental pressures.

    In the standard terminology, neutral or near neutral variation is not cisible to selection. It can propagate or be lost, or just stay in some indivisuals. All that is random variation again.

    Well, be careful of that word “random”. But yes, drift is a stochastic process, that is biased in favour of traits that work, at which point we call it “selection” (misleadingly IMO).

    Yes. That, in stanbdard terminology, is positive natural selection: the expansion of naturally selectable traits, whose effect is to potentiate (higly, I would say) the probabilistic resources that a naturally selectable trait may be a step to further evolution.

    Well, I think that is a very overcomplex way of putting it. Why not just say that where a trait tends to enhance the probability of reproductive success it will become more prevalent in the population? That’s all that’s going on. You don’t need to talk about “potentiating probabilistic resources”, and my concern is that that kind of terminology (like “natural selection”) produces more heat than light. Or more smoke than light!

    Yes. That, in stanbdard terminology, is negative natural selection: the elimination of heavily non functional variation, whose effect is to fix existing functional information.

    Yes, but it isn’t “two kinds of selection”: it’s all differential reproduction relative to the average, and what is better than average in one generation may be worse than average in the next. So splitting it up into two “kinds” of process is potentially very misleading.

    That’s why it is called the “necessity part” of the algorithm.

    Well, if that’s the only reason you are calling it that, then fair enough. But I think it isn’t. You seem to be putting all the stochastic stuff on the variance creation side (even though some of that is highly “necessary”) and all the necessary stuff on the selection side, even though selection is highly stochastic.

    That is, positive NS and negative NS. And so?

    And so it’s a useless concept! There is differential reproduction. Period. If a trait confers greater than average reproductive success in one generation, but less than average in the next, which do we call it? There may be some, very limited, contexts in which it’s a useful concept, I guess, but it certainly needs to be taken with a very large pinch of salt, because the underlying reality it describes is very much simpler: heritable traits confer differential reproductive success in any given environment.

    That’s it.

    And both the generation of variants and differential reproductive success are process with probability distributions in which some events (near-neutral variants; successful reproduction associated with normally beneficial traits) are very much more likely than others (disastrously deleterious or miraculously beneficial variants, unsuccessful reproduction with normally beneficial traits or successful reproduction with normally deleterious traits).

    In other words trying to split “Chance” from “Necessity” is pretty well nonsense, pace Monod (whose book is nonetheless excellent in a heavily French way).

  189. GinoB:

    That’s not what the papers showed. They showed the effects on fitness of variations and showed the effects to be independent of ‘need’.

    OK. You quoted two papers showing trivial examples of simple random variation, and their effects on fitness, obviously independent of need. I still wonder why.

    You have also demonstrated that you still don’t understand it.

    Well, this is a good argument, indeed!

    No one says it does, especially since your ‘dFSCI’ metric is a worthless made-up buzzterm not recognized by or used in the actual scientific community.

    Or, if simple aggression does not work, a call to conformistic thought certainly will…

    Your Point b) strawman is definitely not true, because there’s no requirement in evolution for every mutation to be positively selectable at every step. It is well documented that neutral mutations can and do accumulate in a population through drift, then combine with other later mutations to provide a reproductive benefit.

    Maybe you should go back to aggression and conformism. With ideas, you don’t seem to do well.

    “there’s no requirement in evolution for every mutation to be positively selectable at every step”

    Obviosuly. Whoever said that? Please read again what I said:

    “RV + NS in principle could, but only if the pathway to the complex information could be deconstructed into steps of low enough functional complexity, each of them naturally selectable”

    Is “steps of low enough functional complexity” the same as “every step” in the darwinist mind? If so, there is really no hope.

    The problem is, the steps that can expand by NS must not be so distant that the transition be completely out of the range of the proibabilistic resources of a realistic biological model. That’s what determines the choice of an appropriate throshold of complexity when computing dFSCI in a specific context (Ah, I apologize. I didn’t mean to discuss worthless made-up buzzterms with you; I will not do that again).

    It is well documented that neutral mutations can and do accumulate in a population through drift, then combine with other later mutations to provide a reproductive benefit.

    And it is well obvious, even if the dumb logic of darwinists will never recognize it, that neutral mutations in no way chanhe the probabilities of a random walk, and neither does genetic drift, because it is a purely random event, and therefore does not change enything. The term “RV” includes all forms of possible random variations, including neutral mutations and genetic drift. And all RV is accounted for and evaluated in the ID model.

    You are attacking a worthless strawman version of the actual scientific theory, which is a major reason no one in the scientific community takes these claims seriously. It’s as simple as that.

    Conformism again, plus a bit of aggression. And the strawman detail, which always gives some glamour…

  190. No, of course not. It’s like that silly precambrian rabbit example.

    Clearly, if we really did find something that looked like a centaur fossil, then palaentologists would be trying very hard to try to figure out what its antecedents were, and how it could possibly have evolved a what looks like a synapsid skull with a mammalian jaw yet belong to a completely different lineage. Ditto with the rabbit.

    The much more important point is that there are no precambrian rabbit fossils and there are no centaur fossils. None. Not a single chimera.

    It is the total absence such potentially viable creatures that makes the case so strong for common descent (not Darwinian evolution; common descent). We do not see crossed lineages, except relatively shortly after speciation events, and in the case of horizontal gene transfer. Neither of these could possibly explain a centaur.

    And before someone leaps in with “convergent evolution” – we are not talking about “convergent” features here, like flippers, or dorsal fins, which have comparable form and similar function but are anatomically completely non-homologous. I am talking an actual centaur, with a man’s torso and a horse’s body. It’s probably a perfectly viable creature (unlike the pegasus), but given that men’s torsos and horse’s bodies have their own branches of the tetrapod lineages, you aren’t going to see them duplicated in some hexapod lineage without the Darwinians having a lot of ‘splainin’ to do.

    Which of course they don’t have to do, because there aren’t any centaurs!

  191. Elizabeth:

    I am afraid there is little hope to understand your position on these points. Indeed, it seems completely specious to me.

    So, just a few clarifications:

    The problem with neutral or near neutral variations is that they do not change the global probabilities of a random walk.

    Let’s make an example, to understand better.

    We have a duplicated gene of, say, 150 AAs. The gene is no more active, and so, according to classical darwnist theory, nature can play with it to “explore” new possibilities. (The agency language is only a joke).

    Now, if a gene is not transcribed and translated, mutations become necessarily neutral: nothing can be selected, either positively or negatively.

    Now, let’s say that we assume that thjorugh random mutations that duplicated gene generates, in some evolutionary time, a new protein domain, completely unrelated to the original one. Well, that’s macroevolution, isn’t it?

    Now, if the two sequences (let’s call A the original, and B the final one) are unrelated at sequence level (let’s say they share no more than 5% AAs, a random correspondence), than the transitionform A to B is a random walk. It is realized through neutral mutations. But the point is, of all the 20^150 possible sequences, if we exclude those “near” A (let’s say with more than 30% homology, which are anyway only a tiny fraction of the total), all the others, the “unrelated states”, have approximately eqal proibabilities to be reached. No kind of random variation can change this scenario. Even if for some random reason some mutations can randomly expand, the probabilities do not change, because all mutations have the same probabilities to expand, or be lost.

    Is that clear?

    Now, let’s go to this statement of mine:

    “Yes. That, in standard terminology, is positive natural selection: the expansion of naturally selectable traits, whose effect is to potentiate (higly, I would say) the probabilistic resources that a naturally selectable trait may be a step to further evolution.”

    You say it is overcomplex. But it isn’t. I believe you have not understood my point.

    My point os exactly in the words: “to potentiate (higly, I would say) the probabilistic resources that a naturally selectable trait may be a step to further evolution”.

    Let’s go again to my example.

    The problem, with neutral evolution, is that the variation does not expand, or if it expands it expands randomly. Therefore, the necessary variation must accumulate in a single clone (genetic drift does change that, but again the problem id that it can expand anything, be it useful, neutral or deleterious to the final result).

    So, let’s leave alone drift for the moment. Let’s say that the gene, being lucky, accumulates three “right” mutations for B. Let’s call this state A1.

    Now, if A1 is not selectable, we are still in the general scenario: a random walk, and very limited probabilistic resources (all the changes must accumulate in the same clone).

    But, if A1 gives a sufficient reproductive advantage, in a short time all the population will bring the A1 gene, and no more the A. So, if the population is, say, 10^12 bacteria, we have increased the probabilistic resources of 10^12. That is something.

    That is the role of positive selection.

    At the same time, negative selection will “protect” those three “correct” aminoacids, and avoid that they are changed again in further variation.

    That is the essence of the algorithm.

    But the problem is, those three changes that give a reproductive advantage, and are threfore selectable, must also be a step towards B, IOWs, they must be “right” for B. And than there must be another selectable step, say, with four more chnges that, added to the first three, give again a selectable protein, and still are a further step to B. And so on, until we get B, 150 AAs aftfer.

    That’s what I mean when I say that the algorithm can work only if all the complex functional proteins are deconstructable into simpler steps. each of them selectable.

    That’s the most I can do to epxlain what I mean. Let’s say I have tried.

  192. Let me try the gpuccio form of scientific analysis:

    1. All biological life forms contain SNARGL. It’s obvious to anyone who isn’t blinded by conformism.

    2. Too bad if you don’t understand what SNARGL is or how to measure it. It’s not my job to provide such pathetic levels of detail.

    3. Intelligent Designers have never been seen to create objects containing SNARGL.

    4. Therefore we can infer that biological life was not created by an Intelligent Designer.

    How’d I do? I bet I’d make a fine ID scientist in the grand tradition of the ID researchers who post their pet ideas here.

  193. William J Murray

    And that’s all I’m asking for: not proof that RM & NS did in fact make the trip; only that they are theoretically (categorically) capable of making the trip.

    What sort of metric could science possibly give you that would meet your expectations? Something like Behe’s ludicrous demand that science provide a detailed list of every last mutation in the 100 million year history of a lineage?

    OK, here’s some **rough** calculations. I’ll even use ‘worst case’ numbers. Humans and chimps have very similar DNA, between 98% and 99% similarity depending of which areas you count. Let’s assume 2% difference. Still, with a size of 2.9 billion base pairs that means lots of changes – let’s say 60 million base pair differences. Let’s further assume that we only get one base pair change per mutation, which is certainly unrealistically low.

    Humans and chimps last shared a common ancestor between 4-8 million years ago. Let’s say 4 million. That means the species had to diverge at an average rate of 15 mutations per year, or 7.5 per year per species.

    Now consider that on average humans have between 150-200 mutations per individual per generation. Let’s assume the low value of 150. If we assume a very small stable population, say 100,000, and a generation time of 20 years we still get an average of 750,000 new mutations per year across the entire population.

    So we need 7.5 per year, but theoretically we can get 750,000 per year. Will that get the elephant over the mountain?

  194. GinoB:

    Well, you certainly make a fine arrogant and dogmatic darwinist.

    My compliments, and have a good life.

  195. GinoB:

    Are you saying that one mutation in 10^5 was the right one, and that explains the evolution of humans?

    Truly amazing. I bow to your deep understanding of science.

  196. kellyhomes:

    Have you ever thought about reading my observations, maybe even thinking a bit about them (I know, I am asking much), and in the end writing down a few wrods here in response?

    Or just decide for yourself of they hold or not?

    (This is a call to individual thinking and judgement, usually considered one of the privileges of human condition, in opposition to the call to conformism and external authority, which seems to be the last resort of my “kind” interlocutors when they have nothing else to say).

  197. The problem is, the steps that can expand by NS must not be so distant that the transition be completely out of the range of the proibabilistic resources of a realistic biological model.

    Fine. Give us a documented historical example of a single step transition that is too distant to be traversed except by design.

  198. Petrushka:

    You already know my answer. The appearance of any new protein domain.

  199. Define “appearance.”

    Demonstrate to me that you know for a fact that protein domains have not precursors.

    I’m not buying the gaps argument, that because we don’t know the exact history, that protein domains were poofed into existence fully formed.

    Stick with facts.

  200. Not sure how you are doing the math, but that would be one in 10^5 out of all neutral or nearly neutral mutations being fixed in the population.

  201. Petrushka:

    Appearance: the presumed level in natural history where a new basic protein domain is observed.

    I know for a fact that mobody has ever shown those precursors. One can always believe they exist. One can believe what one likes. I stick with known facts.

    Feel free not to buy what you call “the gaps argument”. We are not in a commercial deal, here. I certainly don’t care for the “poof” pseudo-argument. Not even as a free offer.

  202. I’ve read and thought about your observations. Mostly you search out the gaps in knowledge that result from the erasure of detailed history.

    Such as the origin of protein domains.

    Having found a gap that is difficult or impossible to fill with detailed history, you insert your own theory as fact: namely that the origin of protein domains required them to be poofed into existence by and unspecified designer.

    You haven’t presented us with a before and after scenario, but I have to assume you know the detailed history of protein domains, and are just teasing us.

  203. Petrushka:

    I’ve read and thought about your observations

    I know. My note, indeed, was to kellyhomes.

    Having found a gap that is difficult or impossible to fill with detailed history

    Let’s say at least 4000 independent gaps…

    you insert your own theory as fact

    No. Never. I propose it as the best explanation.

    You seem to forget that it is darwinists who like to label theories as facts. It is really true that one often sees his own sins projected in others…

    I am fond of my epistemology. Many times here I have raised the point that theories are always theories, and facts are always facts, and that a “theory becoming a fact” is not a social promotion, but simply an epistemological horror.

    I know you like to attribute to me many things I have never said, but please, at least don’t do that with the things I have always explicitly fought.

  204. The gist of the paper is that so far the overwhelming number of adaptive (that is, helpful) mutations seen in laboratory evolution experiments are either loss or modification of function.

    Three of 17 in the study were gain of function, and of course the study covers a microscopic slice of time.

  205. Appearance: the presumed level in natural history where a new basic protein domain is observed.

    That’s gobbledygook. Give me an example of the observation of a new protein domain. What does “observed” mean?

    What assumptions are you making about the history of the sequence? What is you evidence for your preferred history?

    What would the before and after snapshot look like?

  206. I propose it as the best explanation.

    Propose what as an explanation for what?

    You haven’t ever said what it is that happened that requires explanation.

    Do you know the history of the origin of protein domains? You have the before and after snapshot? You assert as a matter of fact that naturalistic explanations are inadequate, but you haven’t said what happened that requires intervention.

    You haven’t even presented a plausible case that there is a discontinuity.

  207. GinoB,

    Natural selection INCLUDES random variation and there isn’t any evidence that NS can create biological complexity.

    You can splain it all you want but you LACK evidentiary support.

  208. Natural selection is DEFINED as the differential reproduction due to heritable random variation…

  209. GinoB:

    The ‘random’ part of the term ‘random mutation’ by definition means random with respect to its effect on reproductive fitness – either beneficial, deleterious, or neutral. Such changes by definition are completely uncorrelated with ‘need’.

    Except for the fact that variation enables fitness- random wrt biology means without planning nor purpose

  210. “if living organisms were designed then it is a safe bet they were designed to evolve evolved by design”

    See why this sounds like theistic evolution to me?

    No- it doesn’t have anything to with TE- apparently you don’t understand TE.

    You take a process which is mechanically understood, demonstrably random with respect to need, and best described as evolution.

    LoL- it is only ignorance that sez random with respect to need and ID is not anti-evolution.

    You assert that is “design by evolution.” Without adding anything else.

    I have added plenty- it is called diected/ intelligent design/ front-loaded evolution and is exemplified by numerous targeted searches.

  211. Nick Matzke:

    Larry Moran is talking about the genomes of humans and other large genomes and how much of the sequence change is under selection vs. neutral. Most of it is thought to be neutral. Amongst other things, this is strong evidence that a lot of these large genomes is junk (another position which Moran argues for).

    Bad news, Nick. This is just in from PhysOrg:

    The research team lead by Georgia Tech Professor of Biology John McDonald has verified that while the DNA sequence of genes between humans and chimpanzees is nearly identical, there are large genomic “gaps” in areas adjacent to genes that can affect the extent to which genes are “turned on” and “turned off.” . . .

    “These genetic gaps have primarily been caused by the activity of retroviral-like transposable element sequences,” said McDonald. “Transposable elements were once considered ‘junk DNA’ with little or no function. Now it appears that they may be one of the major reasons why we are so different from chimpanzees.”

    Another day; another bad day for Darwinism! ;)

  212. Petrushka:

    You know well, but your job seems to be to ask again and again.

    Thew appearance of 4000 independent functional protein domains in the course of natural history, without any trace of precursors, certainly requires explanation. Except for you, it seems.

    You are free to decide if my case is palusible or not. Anyway, I have presented it.

    Your repeated asking is obviously mere propaganda. You have asked. I have answered. You are not satisfied. OK. All that is fine. Now, please, don’t ask again the same things. You will not get a different answer.

    Maybe you will not get any answer.

  213. gpuccio

    You seem to forget that it is darwinists who like to label theories as facts.

    No one in the scientific community labels theories as facts.

    It’s exactly that kind of dishonest comment on your part that makes your integrity so suspect.

  214. GinoB:

    From Wikipedia:

    2Fact is often used by scientists to refer to experimental or empirical data or objective verifiable observations.[13][14][15][16] “Fact” is also used in a wider sense to mean any theory for which there is overwhelming evidence.
    A fact is a hypothesis that is so firmly supported by evidence that we assume it is true, and act as if it were true. —Douglas Futuyma[17]
    Evolution is a fact in the sense that it is overwhelmingly validated by the evidence. Frequently, evolution is said to be a fact in the same way as the Earth revolving around the Sun is a fact.[17][18] The following quotation from H. J. Muller, “One Hundred Years Without Darwin Are Enough” explains the point.
    There is no sharp line between speculation, hypothesis, theory, principle, and fact, but only a difference along a sliding scale, in the degree of probability of the idea. When we say a thing is a fact, then, we only mean that its probability is an extremely high one: so high that we are not bothered by doubt about it and are ready to act accordingly. Now in this use of the term fact, the only proper one, evolution is a fact.[3]
    The National Academy of Science (U.S.) makes a similar point:
    Scientists most often use the word “fact” to describe an observation. But scientists can also use fact to mean something that has been tested or observed so many times that there is no longer a compelling reason to keep testing or looking for examples. The occurrence of evolution in this sense is fact. Scientists no longer question whether descent with modification occurred because the evidence is so strong.[19]“

  215. GinoB:

    (always form Wikipedia):

    R. C. Lewontin wrote, “It is time for students of the evolutionary process, especially those who have been misquoted and used by the creationists, to state clearly that evolution is a fact, not theory.”[25]

    Douglas Futuyma writes in his Evolutionary Biology book, “The statement that organisms have descended with modifications from common ancestors—the historical reality of evolution—is not a theory. It is a fact, as fully as the fact of the earth’s revolution about the sun.”[12]

    Richard Dawkins says, “One thing all real scientists agree upon is the fact of evolution itself. It is a fact that we are cousins of gorillas, kangaroos, starfish, and bacteria. Evolution is as much a fact as the heat of the sun. It is not a theory, and for pity’s sake, let’s stop confusing the philosophically naive by calling it so. Evolution is a fact.”[26]

    Neil Campbell wrote in his 1990 biology textbook, “Today, nearly all biologists acknowledge that evolution is a fact. The term theory is no longer appropriate except when referring to the various models that attempt to explain how life evolves… it is important to understand that the current questions about how life evolves in no way implies any disagreement over the fact of evolution.”[4]

  216. I’m going to slightly disagree, GinoB :)

    Let’s drop the word facts, and substitute “data” – literally “what we are given”.

    All data are observations, and all observations are, at some level, models. An average, for example, is a model; a measurement, even, at some level is a model. And what are data at one level can be models at a level below.

    I’m very aware of it in my field because my data are quite highly derived. In fMRI the “image intensity” data I analyse are actually outputs from a more basic model in which something quite different is the input and “image intensities” are the models that best fits the data.

    But that’s just a “fact” of life :) All of our observations are approximations, “best guesses” if you will, even if the “best guess” is very close indeed.

    But I do agree that no-one labels a “theory” – or any other model – as a “fact”. We certainly make predictions based on the assumption that certain well-supported theories are true, but assuming something is true is not the same as regarding it as a fact.

    There are no “facts” in science, there are simply models and data, and data at one level are models at another. What tells us our models are likely to be accurate is how well each model fits the data it models at every level. Another thing that tells us our models are likely to be accurate is consilience between inferences derived from very different models of independent data. That’s how we can be so sure that YEC is wrong, for instance.

  217. GinoB:

    You may also see how many bold statements about evolution grossly conflate neodarwinain evolution and common descent.

    Luckily, that is irrelevant to this discussion about my integrity. Indeed, both neodarwinism and common descent (and, obviously, ID) are certainly theories, and not facts.

  218. gpuccio

    GinoB:

    From Wikipedia:

    Exactly as I said, no one in the scientific community labels theories as facts.

    That only happens with ignorant laymen, or intellectually dishonest scoundrels with an agenda to push.

    Which one are you?

  219. gpuccio

    Luckily, that is irrelevant to this discussion about my integrity. Indeed, both neodarwinism and common descent (and, obviously, ID) are certainly theories, and not facts.

    Wrong.

    “Neodarwinism” is a theory.

    Common descent is a fact.

    ID is an unsupported hypothesis.

    Don’t play at science if you don’t understand the terminology.

  220. Elizabeth:

    I agree in general with much of what you say here. And still, I think that a separation between observables (facts) and inferences (theories) must be kept.

    Let’s take a measure, for instance. It is true that it is an approximation, and it is true that it implies many concepts (such as the concept of number) that go well beyond the physical act of measuring.

    But still, the measuring is a fact, an observable. It is not an inference.

    Inferences make statements about things that we are not certain of. Especially, they try to explain things. An explanation is never an observable. It is always an inference.

    So, with all the due attention to the problems you point to, I would definitely maintain a strict separation between facts and theories.

    One important point is: facts are not always certain. In a sense, facts are facts, and therefore real. But we must rememebr that we know facts thorugh observation. And our observation of facts is not always correct, or reliable.

    But explanatory theories are all another set of things.

  221. GinoB

    The way archaeologists determine if a find is human produced (say a primitive stone ax) or just a natural rock is by comparing the object with other known human designed similar objects. Not superficial similarities, not analogies (like flagella and outboard motors) but actual known designed objects. They don’t just look at the rock itself but look for other signs of manufacture, things like specific chipping patterns, flint flakes, a work area where the tool was produced, and the source of the material. They also go to great lengths to identify the likely designer – who was living in the area at the time, what was their level of technology at the time, etc.

    The whole ID party line “it’s not about the designer, just the design” is one of the most intellectually vacuous bits of nonsense that’s ever come down the pike.

    Archaeologists compare those items to known, like items and identify designers because they can. That information is readily available and there is plenty of evidence to make sound judgments on those types of things. To my knowledge, we have no physical evidence or observations for who the designer(s) could have been. I think ID skeptics say what you say (that it is “vacuous” to not address the identity of the designer) because you know it is currently impossible to do so without speculation or faith.

    But archaeologists DON’T need to know who the object came from or have other known designs of that specific type of object in order to declare an object designed. They can find any object, observe patterns that closely resemble those of a known human manufacturing method, and if no other sources of those patterns in the natural world are known (such as erosion, animal behavior, impacts, etc.) then they can infer design without any further knowledge. Inference to the best known explanation. The process does not stop there for archaeologists, of course, because they usually have other information they can work from, and identifying designers, uses, etc. is generally much more interesting to their field than simply identifying objects as natural or man made.

    It would be thrilling to be able to scientifically talk about the identity of the designer, but from our current observations that is not possible. That doesn’t mean we can’t infer design. Your assertion that that is intellectually vacuous is either willfully misrepresentative or carelessly ignorant. Unless you can explain why an archaeologist needs to know the identity of the people who created a tool in order say that the tool was designed, your assertions remain unsupported

    Imagine that we find an object deep in the Antarctic ice that is made from materials we’ve never seen, has seemingly specified contours and performs amazing activities like hovering, cold fusion, etc. We would have no idea how it was made, who made it or what it is for, but we would know that it was designed. So your asserted archaeological design-detection process would fail. (Note: I am not saying that this is ID, to just look at biology as see that it is obviously designed. I’m just pointing out the fallacy that is your made-up design-detection requirements of archaeologists.)

  222. Yes, I think it is true that “neodarwinism” (still not sure what that means!) and “common descent” are conflated.

    Common descent is strongly indicated by the distribution of anatomical features in living things (if plants and bacteria can be said to have “anatomy). Evolutionary theory is model that explains the common descent model of that distribution.

    But evolutionary theory could also apply to, for example, a YEC model, in which Darwinian mechanisms apply to post-Ark radiation, but there is no universal common ancestor.

    Similarly, common design could explain nested hierarchies without invoking common descent.

    And ID could be a guiding factor in guiding evolution down the lineages from a universal common ancestor, without Darwin’s theory having to be true.

    So falsifying Common Descent wouldn’t falsify Darwinian evolution, nor would falsifying Darwinian evolution falsify Common Descent.

    That said, the evidence for Common Descent seems to me even more overwhelming than the pretty overwhelming evidence for Darwinian evolution as an explanation of Common Descent!

  223. GinoB:

    Common descent is a theory. A theory I agree with, but a theory just the same.

    Have you observed common descent of species? And universal common descent? Have you observed LUCA?

    Npo. Those are only inferences. Starting form many facts, an inference is made (a good inference, IMO), that living species we observe now are derived from a common ancestor.

    That is a theory.

  224. Elizabeth:

    I agree in general with much of what you say here. And still, I think that a separation between observables (facts) and inferences (theories) must be kept.

    Yes indeed. My point is that they need to be rigorously ranked rather than separated, but in practice, at any given level, we can separate what is given (literally, “data”) from what we infer (our model).

    Let’s take a measure, for instance. It is true that it is an approximation, and it is true that it implies many concepts (such as the concept of number) that go well beyond the physical act of measuring.

    But still, the measuring is a fact, an observable. It is not an inference.

    Sure, for all practical purposes, anyway. Though you ignore “measurement error” at your peril!

    Inferences make statements about things that we are not certain of. Especially, they try to explain things. An explanation is never an observable. It is always an inference.

    Well, no. Your measurement is still an inference, even though you have just called it a “fact”. As it happened, I just measured the window embrasures in our spare bedroom in order to make extremely close-fitting acoustic baffles so that my son can practice his brand new souped-up drumkit in there! And I am very aware that “991mm” is an inference from the fact that my father and I measured it several times and got 990mm, 992mm, and 989mm. So I’m still being nickety pickety here.

    But I do agree that a “mean” or some other kind of summary value is only a “model” in a very specialist sense, and is not an “explanatory model”. We should not call “explanatory models” facts. Does that put us on the same page?

    So, with all the due attention to the problems you point to, I would definitely maintain a strict separation between facts and theories.

    One important point is: facts are not always certain. In a sense, facts are facts, and therefore real. But we must rememebr that we know facts thorugh observation. And our observation of facts is not always correct, or reliable.

    But explanatory theories are all another set of things.

    We agree :)

    Cool.

  225. Thew appearance of 4000 independent functional protein domains in the course of natural history, without any trace of precursors, certainly requires explanation.

    Do you have a reference for this?

  226. Elizabeth:

    We should not call “explanatory models” facts. Does that put us on the same page?

    Yes! Cool. :)

  227. Elizabeth:

    For the appearance, I think there is much. I usually refer to the paper I have already linked. I do it again:

    http://www.plosone.org/article.....tation=PDF

    Please refer in particular to Table 1.

    For the lack of known precursors: I have been asking examples of precursors for years. Nobody has ever given one.

    About the number of basic protein domains, I want to make a clarification.

    I refer to numbers from the SCOP classification of the known proteome.

    You can give different numbers according to the level of definition, but essentially the concept is the same.

    So we have:

    Folds: 1195

    Superfamilies: 1962

    Families: 3902

    Sequences with less than 10% identity: 6311

    Sequences with evalue > 1: 6680

    So, we have separated groups in a number of about 1195 – 6680, sequences completely separated in the sequence space, without any identity beyond random, and in most cases with no structural similarity.

  228. I have to say, I’m not understanding your interpretation of that paper.

  229. DrREC

    You believe the gene presented above is designed. How would I falsify that? Be specific.

    You’re right that you absolutely cannot falsify someone’s belief that something is designed. Say I’m on a beach and decide I want a specific grain of sand to rest in a certain location on the beach; I move it there, precisely as I wanted. Then you walk up. I say that the location of that grain of sand is designed. You do not believe me because you can show me that natural forces (wind, water, etc) are adequate explanations of such a phenomenon. ID is defeated in this instance (even though it actually was designed!) because the inference to the best explanation results in a probabilistically viable natural explanation. You still cannot prove that I did not design the location of that sand granule, but you can refute an actual design inference based on available observations. If someone recorded me placing the granule there, then the design inference is satisfied.

    The problem with theistic evolution is that it is like trying to say the beach was designed even though it is 100% indistinguishable from a natural beach. It is a pointless assertion. I think many theistic evolutionists are unwitting ID advocates. I’ve heard many of them talk about “guided” evolution…that is ID. Either it’s guided or unguided; even if only 1% of its history was guided, it is still guided. They are saying it is at least somewhat guided, yet it is still 100% natural (i.e. unguided). It is simply self-contradictory.

  230. What all these comparisons with found-objects (including Paley’s watch) is that the found-objects don’t reproduce themselves.

    Obviously if you find an object that looks designed to do something, then your first question is: what might it have been designed to do?

    And if it looks like an instrument of some sort, or an implement, you ask who might have used it to do that thing.

    But if it’s a self-reproducing object, and it looks designed to enable itself to reproduce, you don’t need to look for someone else who might have designed it for their own purposes, you can see straight away that it is of use to itself in the task of reproducing itself.

    Which means that it’s capable of Darwinian evolution, because Darwinian evolution simply states the obvious that if a self-replicator replicates with heritable variation in reproductive success, variants that are best at reproducing themselves will become most prevalent.

    Now, it could still have been “intelligently designed”, but that is no longer the only inference we can make. We now have an alternative mechanism – one tends to maximise reproductive success.

  231. “Chance” does not “drive” anything, kf.

    You made this point quite eloquently yourself recently.

    Chance is simply the word we use when something has a probability of less than one, given well-specified conditions (as most things do, in fact).

    Much better to talk of probability distributions. The probability distribution of mutations by selection coefficient is by no means flat. In other words mutations are not “random” in the common-or-garden sense at all. Near-neutral mutations are much more likely than extreme mutations, and extremely deleterious mutations, even if they happen, are very unlikely to propagate to many, if any, offspring.

    So “random mutation” is a misnomer. Mutations aren’t “random” at all, but they are drawn from a non-flat probability distribution. Similarly, differential reproduction is neither “random” nor “non-random” in the common-or-garden sense either. An organism’s probability of replicating may be slightly higher than average if, for example, it has better than average camouflage, but it could still be stamped on or drown.

    So both “rm” and “ns” are highly stochastic processes, and neither are “random” in the usual sense of the word. So even “blind” and “undirected” are poor words to describe “rm+ns”. Variants that work are generated in preference to variants that don’t (in other words the variance-generation mechanism isn’t entirely blind, and favours variants that sort-of-work), and differential reproduction is biased in favour of phenotypes that manage to stay alive long enough to find a mate and breed successfully.

    Be careful the metaphors don’t wag the dog.

  232. How would you know it is an ancient alien spacecraft, unless it resembles spacecraft constructed by humans?

    I ask this in all sincerity, because there are numerous stone formations cited as lost cities and such by some investigators. Many are controversial.

    When you encounter an ambiguous structure you have to ask if it has key features found on objects known to be made by humans or animals. At the same time you also ask if it resembles things formed by natural processes. Sometimes, as in the case of stone tools, there are disputes over interpretation.

    The problem with interpreting living populations as designed is that we have a candidate for a natural process that produces incremental change over time. We have no candidate for a designer capable of anticipating the results of sequence changes in DNA. The large numbers cited as as evidence of design also make anticipation of genetic change impossible. there simply isn’t any way, even in principle, to anticipate changes in protein folding or regulatory sequences.

  233. Chance circumstances and factors that follow stochastic patters do play a factor in many proceedings, so to say that chance variation and natural selection lead to descent with mods is a fair summary of the basic darwinian frame.

    I agree that natural selection has a stochastic component, but that does not change the dynamics: the selection is negative, elimination of some variants.

    That leaves chance variation as what has to write the complex digital code we find in body plans.

    Which simply does not add up.

    The dominant Darwinian Scheme may explain adaptations of varieties within body plans, but it does not properly explain the origin of basic body plans.

  234. A specification is independent of the particular implementation, and defines a zone of interest T in the config space, where we find particular outcomes E; and, specifications can be deduced from reverse engineering and routinely are. Biofunction in particular ways is a valid specification, and demonstrably occurs in various ways since each organism within a species is an individual.

  235. I agree that natural selection has a stochastic component,

    cool :)

    but that does not change the dynamics: the selection is negative, elimination of some variants.

    Selection is just heritable differential reproduction. Some new variants will result in phenotypes that reproduce better than the average of their peers, some worse. Those that reproduce better will tend to become more prevalent; those that reproduce worse will tend to become less prevalent. Most new variants will fare just the same as all the others, and may or may not be drift through the population.

    It isn’t any truer to say “selection is negative” than to say “selection is positive”. What there is is variance in reproductive success.

    That leaves chance variation as what has to write the complex digital code we find in body plans.

    Please let’s leave “chance” out of it, for reasons you yourself gave! It leaves a probability distribution for what new variants will appear that is strongly biased in favour of variants that basically work. Within this narrow range of possible variants, the variants that actually occur, the probability of one that results in a successful body-plan variant (bilateral symmetry for example) may be quite high.

    If bilateral symmetry turns out to be advantageous, future variants will be highly constrained (i.e. not “random” in the common-or-garden sense) to variants on bilateral symmetry. Front and back ends, for instance. Now you have the beginning of hox genes. Rinse and repeat.

    But remember that what you are calling “Chance” is by no means an equiprobable draw. Genetic variants that are produced are highly constrained to produce phenotypic variants close to the already-successful parent variant.

    It’s “Chance” as in drawing a three digit number from a barrel of tickets numbered 1 to 1000, not “Chance” as in drawing ticket number 327.

  236. Elizabeth:

    What is it that you don’t understand?

    Table 1 lists the levels at which new domains emerge.

    1984 out of 3464 are already present in LUCA (before separation of archaea and bacteria).

    31 appear after in Archaea (13+14+4).

    144 + 9 + 2 + 2… appear in bacteria

    And so on.

    For instance, the 492 listed as Eukaryota are domains specific to eukaryota, therefore more recent than the oroigin of Eukaryota, but not much more recent, because they are common to all of them.

    58 new domains are common to all metazoa, and others originated later, in specific phyla (15, for example, common to chordata).

    There is no special interpretation. This is just a reasonable timeline of when new domains emerge in the proteome.

  237. No one disputes evolution is capable of adapting existing species. But evidence suggests it can’t do more than that. Evidence suggests that evolution is not powerful enough to produce new species.

    What “evidence suggests that evolution is not powerful enough to produce new species”?

    And by “new species” do you the subdivision of a single population into two non-interbreeding populations, of which one may resemble the original population more closely than the other? In which case why not? The evidence from island populations seems very powerful in this regard.

    Or do you mean longitudinal functional change in a population that exceeds some threshold? In which case, what threshold?

  238. Elizabeth:

    I fully agree with your 43.1.1.1.10 (I will never get accustomed to this kind of nested hyerarchy!).

    I would only rephrase the last sentence as follows:

    “That said, the evidence for Common Descent seems to me overwhelming enough, while the evidence for Darwinian evolution as an explanation of Common Descent is completely lacking!”

    By the way, my personla reason for believing in CD is, just to stay consistent, molecular. I don’t love fossils and similar, but the pattern of homologies and differences between similar proteins in different species is very convincing, IMO, at least of some physical reutilization of the code in the development of design.

  239. uoflcard @ 24.1.1.1.4

    “You’re right that you absolutely cannot falsify someone’s belief that something is designed.”

    Therefore, ID is not science. It is a belief tacked onto science.

    “ID is defeated in this instance (even though it actually was designed!) because the inference to the best explanation results in a probabilistically viable natural explanation.”

    Above, I reference a study showing a gene evolving by apparently natural processes, which are demonstrably random with respect to need. It creates a new functional protein. Is ID not defeated in this case because I’ve demonstrated a viable natural explanation for creation of new information? And secondly, where is the design inference? Is a long process, random with respect to need, comparable to human design?

    “You still cannot prove that I did not design the location of that sand granule, but you can refute an actual design inference based on available observations. If someone recorded me placing the granule there, then the design inference is satisfied.”

    As I’ve said before, the design inference is without empirical support. Has anyone recorded the designer creating improbable amounts of information at once? I was chuckling at KF’s “you weren’t there” reply on the comment thread he closed. I was preparing a response, but I guess he wasn’t wanting to hear it.

    “The problem with theistic evolution is that it is like trying to say the beach was designed even though it is 100% indistinguishable from a natural beach.”

    And what did ID say about the gene above? Looks like 100% natural process that yielded new information, but nah, it must be designed? That is JoeG’s approach it seems. Thats why it seems like in the details ID=TE.

    “It is a pointless assertion. I think many theistic evolutionists are unwitting ID advocates”

    Agreed, ID devolves to TE, and probably vice-versa.

    “I’ve heard many of them talk about “guided” evolution…that is ID”.

    Yep. Same thing. Neither adds anything to the natural study of the history of life, just superfluous add-ons, like adding Pat Robertson’s theory of Katrina to a meteorology class. Scientifically useless, divisive and silly.

  240. I don’t know what you mean by “Thew appearance of 4000 independent functional protein domains in the course of natural history, without any trace of precursors, certainly requires explanation.”

    That paper derives a family tree in which the lineage in which each new protein domain first appears is given.

    Is your problem that there is no “precursor” to each new domain? Or is it that 1984 domains were already present in our Last Universal Common Ancestor?

    If the second, why is that especially a problem? It just means that being the Last Common Ancestor, we have no extant species with which we share an earlier ancestor! So by definition, with this technique, we can only go back as far as the last node.

    If, by amazing good fortune, we discovered some extant population of critters that with which all extant species had a lot in common, but which had protein domains not found in the current LUCA, and lacked protein domains found in the current LUCA, then the new postulated LUCA that included the new population would be an earlier organism than the current LUCA. In which case that 1984 would be revised downwards.

    Not that that is likely but there are still habitats unexplored on the earth’s surface so it’s possible.

    But my point is that the LUCA is only the LUCA of the sampling of lineages for which we have genetic evidence. That is a very small subset of all lineages, so we should certainly not expect the LUCA to be the LUCA of all the unknown lineages, and we should certainly expect there to be a rather large lump of accrued domains sitting at the LUCA, unless, indeed it was also the FUCA.

    In which case we might still expect to see that lump! But we certainly can’t infer that it was!

  241. Elizabeth:

    I quote that paper, indeed, for two different reasons.

    In the context of this last discussion, I was referring to it because:

    a) I had said: “The appearance of 4000 independent functional protein domains in the course of natural history, without any trace of precursors, certainly requires explanation.”

    in response to some other person, and you asked:

    “Do you have a reference for this?”

    My answer:

    “For the appearance, I think there is much. I usually refer to the paper I have already linked. I do it again:

    http://www.plosone.org/article…..tation=PDF

    Please refer in particular to Table 1.

    For the lack of known precursors: I have been asking examples of precursors for years. Nobody has ever given one.”

    So yes, for this discussion the paper is useful in the sense that it gives a cronological order of appearance of the domains, and allows us to determine where they appeared (in what beings).

    That was my reference for “The appearance of 4000 independent functional protein domains in the course of natural history”.

    The important point is that new domains appear throughout natural history, even if with constantly decreasing rate.

    The lack of known precursors is self-evident, but if you are aware of them, please let me know.

    The second reason that I quote that paper (and I have done, with you) is that I find really amazing that more than half of those domains were already present in LUCA.

    Now, I understand all your discussion about LUCA, but you seem to underestimate a very simple concept: as far as we know, and according to what is currently believed, LUCA lived a lot of time ago, probably only a few hundred million years after the formation of earth, or at least the moment earth became compatible with life. IOWs, LUCA is not too distant from OOL, whenever it happened.

    I still think it is amazing that 1800 protein domains originated in such a short evolutionary time.

    And let’s say there was a FUCA. It is still amazing that we have no trace of it. IOWs, it is really amazing that all the supposed evolution from a simple FUCA to a very complex LUCA, while generating such a trasure trove of protein information, apparantly happened without any fundamental separation of living beings, and that the first radical separation was that between archaea and bacteria.

    That’s why I don’t believe in FUCA.

    At the same time, I am all for a parsimonious theory of the emergence of protein domains.

    If some explanatory mechanism can be invoked for the span: OOL – LUCA, and the emergence of almost 2000 domains, there is no reason to think that another explanation should be invoked for the remaining domains that appeared after.

    IOWs, one explanation is the parsimonious choice. Either neodarwinian evolution, from OOL to LUCA and after. Or design.

    Guess my choice?

  242. The important point is that new domains appear throughout natural history, even if with constantly decreasing rate.

    The lack of known precursors is self-evident, but if you are aware of them, please let me know.

    What would a precursor actually be? I would assume that it would be a gene sequence that was close to coding for a new stable domain, possibly being an existing domain itself.

  243. I still think it is amazing that 1800 protein domains originated in such a short evolutionary time.

    Well one explanation would be that early replicators are likely to have had a much higher mutation rate – great for exploring protein space but bad because a high proportion of offspring would be non-viable. A selective advantage would exist for replicators that were better at reducing error rates, resulting in less exploration of protein space, and less discovery of new domains, but more offspring (and consequently less energy cost when reproducing). This could explain the high rated of domain discovery at first followed by reducing rates later.

  244. DrBot:

    A precursor would be a domain intermediate between a previous existing domain and the new one, and functional. IOWs, some trace of a gradual transition.

    Instead, domains are well separated functional islands.

    And anyway, thank you for trying some answers. I appreciate that. I am not impressed, but at least you tried.

    Answers are always good, because thay can be discussed and tested.

  245. Why do they have to be functional? All that really matters is that they are not too detrimental.

    And anyway, thank you for trying some answers. I appreciate that. I am not impressed, but at least you tried.

    Thanks for your kind words – I’m not impressed by you either! ;)

  246. domains are well separated functional islands.

    What methods did you use to determine this?

  247. DrBot:

    How would you consider sequences sharing less than 10% identity, and with different structures and functions?

  248. Do all domains share less than 10% identity?

  249. DrBot:

    Please look at my post 44.1.1.

    If ypou go on the SCOP (Structural Classification of Proteins) site, you can access a tool called ASTRAL. By that tool you can ask for the identifiers of domains sharing less than n% identity. 10% is the lowest value you can set.
    You get 6311 identifiers that way.

    A classification based purely on fold structure, much more conservative, gives 1195 independent folds.

    Superfamilies and families are intermediate classifications.

    The evalue search gives results similar to the % of identity search setting an evalue >1 (no statistically significant homology for sure): 6680 independent groups.

    Obviously, not all domains have less than 10% homology. Protein families include often many domains that are quite similar. That’s why I always speak of “basic protein domains”, that is those groups that are really independent (1195 – 6680 according to the grouping one chooses).

    For instance, the paper I am referring to uses a classification based on 3464 domains, that is the munber of protein families in SCOP 1.73 (there are 3902 in SCOP 1.75, the most recent).

  250. Thanks, I’ll take a look at SCOP.

  251. DrBot:

    Why do they have to be functional? All that really matters is that they are not too detrimental.

    No, the intermediates whose traces we should find are those that were positivley selected and expanded at some time. Theresore, those functional. Indeed, more functional then their precursors.

    IOWs, the point is:

    a) We have a domain that apperas for the first time (B).

    b) To explain that by neodarwinian mechanisms, we need some precursor (A), previously existing, that by RV and NS gave the result of the appearance of B. The only alternative would be that the transition from A to B was merely by RV, that is neutral mutations and drift and similar. But, as both A and B are unrelated long molecules, that is practically impossible: the probabilities are completely against that, and any good neodarwinist knows that.

    c) Therefore, we need some intermediates (for simplicity, let’s assume one and call it A1; indeed, there should be a lot of them for each transition).

    d) The idea is that A1 was naturally selected and positively expanded. Otherwise, no help would be gained against the probabilistic wall of a purely random transition.

    e) Rgerefore, A1 had to be functional. Indeed, more functional than A, to be expanded.

    e) Well, the problem is, in the existing proteome, we have A, we have B, but no trace of A1.

    Now, I have tried to express this problem, that I would call the lack of molecular intermediaries between existing basci domains, to serious darwinist friends. Their answers are speculative, vague and non credible (not their fault, the problem is what it is, and IMO non solvable in darwinian terms).

    The usual explanation if thatthose transitions happened in the past, and that for some strange reason all the intermediaries were cancelled afterwards.

    Now, I could admit that in some cases (although I find it a very bizarre explanation anyway), but certainly not in all cases.

    So, observing the existing proteome, and if we want to explain it forcibly in neo darwinian terms, the only viable hypotheses would be:

    1) All basic protein domains, or most of them, were generated by pure RV.

    or

    2) There is some strange law of nature that erases systematically all molecular intermediaries between basic protein domains, although they were functional enough to be naturally selected and expanded at the time they served as intermediate steps to the transitions.

    I’m not impressed by you either!

    Fair enough! :)

  252. e) Well, the problem is, in the existing proteome, we have A, we have B, but no trace of A1.

    Do we? I know of no such example. Please elaborate.

    e) (the first e, you have 2) is also false, but whatever.

  253. DrREC:

    Do we? I know of no such example. Please elaborate.

    You have to follow the whole reasoning to understand the statement.

    The reasoning was:

    We have domain B emerging at some definite point in natural history. We are trying to explain it not as a result of pure RV, but as a result of a transition form some already existin, unrelated domain, through selectable intermediate steps.

    So, it is already in the assumption that A and B are domains we can observe in the proteome. A can be whatever domain we hypothesize as a precursor. A and B are unrelated, because all basic domains are unrelated, and B originates at a specific time, and there is no trace of related sequences in beings that appeared preciously.

    So, the basci points are that we need to hypothesize molecular intermediaries, functional and selectable, if we want to explain B with a darwinian transition from any existing domain A. And there is not trace in the present proteime of such intermediaries (A and B are separated unrelated domains, and no sequence is known that is a bridge between them).

    e) (the first e, you have 2) is also false, but whatever.

    Why? Please, elucidate.

    The statement is:

    “Therefore, A1 had to be functional. Indeed, more functional than A, to be expanded.”

    Why is it false? Remember that we are discussing a model where NS intervenes, not a model of pure RV (including neutral mutations and drift).

    In a model based on RV + NS, the selected triat has to expand, to gain real advantage versus a purely random model. As I have explained, it’s expansion that multiplies the probabilstic resources. Without expansion, you are still in the random situation.

    So, what is your point?

  254. No, the intermediates whose traces we should find are those that were positivley selected and expanded at some time. Theresore, those functional. Indeed, more functional then their precursors.

    There is some strange law of nature that erases systematically all molecular intermediaries between basic protein domains, although they were functional enough to be naturally selected and expanded at the time they served as intermediate steps to the transitions.

    You are forgetting about neutral drift.

    You are also falsely claiming that the precursors need to be functional. They don’t.

  255. DrBot:

    You are forgetting about neutral drift.

    But… have you at least read my post 47.1.1, to which you are apparently responding?

    I quote myself:

    “Why is it false? Remember that we are discussing a model where NS intervenes, not a model of pure RV (including neutral mutations and drift).

    In a model based on RV + NS, the selected triat has to expand, to gain real advantage versus a purely random model. As I have explained, it’s expansion that multiplies the probabilstic resources. Without expansion, you are still in the random situation.

    So, what is your point?”

  256. Why is it false? Remember that we are discussing a model where NS intervenes, not a model of pure RV (including neutral mutations and drift).

    In a model based on RV + NS, the selected triat has to expand, to gain real advantage versus a purely random model. As I have explained, it’s expansion that multiplies the probabilstic resources. Without expansion, you are still in the random situation.

    Umm, OK, so you are using a model that does not apply to Biology.

    Near neutral ‘traits’ can accumulate in a population – the population can drift.

    Look at it this way, if a neutral mutation or other genetic alteration occurs in an organism that is otherwise reasonably fit (produces offspring) then that neutral change can get passed to the offspring, and so on – those neutral changes can spread through a population.

  257. If ypou go on the SCOP (Structural Classification of Proteins) site, you can access a tool called ASTRAL. By that tool you can ask for the identifiers of domains sharing less than n% identity. 10% is the lowest value you can set.

    One problem there is it is only comparing protein coding sequences. To get a full picture of the degree of isolation between domains you need to look at non-coding sequences as well because these can potentially provide routes between domains.

  258. And there is not trace in the present proteime of such intermediaries (A and B are separated unrelated domains, and no sequence is known that is a bridge between them).

    You are making several unwarranted assumptions.

    One false assumption is the we have sequenced a significant percentage of existing genomes and can reliably judge whether domains are truly isolated.

    Another assumption is that domain sequences do not change over time due to drift.

    Another assumption is that there never were links and that no linking sequences have become extinct. We of course know that extinction doesn’t happen. (Question: what would the status of Australian marsupials be without fossil evidence in South America?)

    But you find it reasonable to believe that invisible fairies poofed domain sequences into existence, fully formed, perhaps from the head of Zeus.

    Now that’s rational. God of the gaps seems to be the only continuing theme in ID.

  259. Which is why neutral drift is so important, of course. Without neutral drift, the Irreducible Complexity argument might have some force. As it is, it doesn’t.

  260. For a neutral mutation to become fixed, 1/4N generations are needed. With N=100,000, that means 400,000 years. So, for 4 million years of divergence, that’s 10 mutations. Now what about the other 59 million, nine-hundred ninety-nine thousand, nine hundred and 90 other needed mutations?

    And, BTW, there’s a new study indicating that it is NC DNA—transposons—that are responsible for chimp/human divergence.

  261. Gino B:

    43.1.1.1.2:

    No one in the scientific community labels theories as facts.

    43.1.1.1.3: gpuccio, in response:

    The National Academy of Science (U.S.) makes a similar point:
    Scientists most often use the word “fact” to describe an observation. But scientists can also use fact to mean something that has been tested or observed so many times that there is no longer a compelling reason to keep testing or looking for examples. The occurrence of evolution in this sense is fact. Scientists no longer question whether descent with modification occurred because the evidence is so strong.[19]“

    Gino B @ 43.1.1.1.7:

    Exactly as I said, no one in the scientific community labels theories as facts.

    Can you read English?

  262. GinoB:

    “Exactly as I said, no one in the scientific community labels theories as facts.

    That only happens with ignorant laymen, or intellectually dishonest scoundrels with an agenda to push.

    Which one are you?”
    ====

    More importantly, which one is Dr Gerald Joyce ???

    “Evolution is not a theory for us chemcists” Dr Gerald Joyce said, “Evolution has now been proven a fact, it’s not just a theory anymore.”

  263. DrBot and Elizabeth:

    Let’s talk about neutral drift. Can neutral drift in any way be called Darwinism, or even, neo-Darwinism?

  264. DrBot:

    Why are you so chaotic in your reasoning?

    Let’s try some order.

    Look at my post 38.1.1:

    “And it is well obvious, even if the dumb logic of darwinists will never recognize it, that neutral mutations in no way change the probabilities of a random walk, and neither does genetic drift, because it is a purely random event, and therefore does not change anything. The term “RV” includes all forms of possible random variations, including neutral mutations and genetic drift. And all RV is accounted for and evaluated in the ID model.”

    and my post 47 (in response to you):

    “IOWs, the point is:

    a) We have a domain that apperas for the first time (B).

    b) To explain that by neodarwinian mechanisms, we need some precursor (A), previously existing, that by RV and NS gave the result of the appearance of B. The only alternative would be that the transition from A to B was merely by RV, that is neutral mutations and drift and similar. But, as both A and B are unrelated long molecules, that is practically impossible: the probabilities are completely against that, and any good neodarwinist knows that.”

    And so on.

    You say:

    you are using a model that does not apply to Biology

    Why? I am using the standard neodarwinian model. RV + NS.

    The RV part includes all forms of random variaiton, including neutral muattions and genetic drift.

    The RV part has the probabilistic power of any random system. With the search spaces we are discussing, it is almost completely powerless, if it has to work alone.

    That’s why we are discussing the NS part, that shouls “help” RV in its impossible tasl, by multiplying probabilistic resources when a selected tract expands. And a transition “helped” by NS implies functional selected intermediaries.

    Is that clear?

    Some more reflections on the reason why drift is non relevant in the computation of probabilistic resources.

    Let’s say that a functional mutation is selected, and expands, for example, in a population, from one original individual to a population of 10^9, say, because of that positive selection. There is no doubt that, if (and only if) that mutation is really a step towards some future complex functional result, then the probabilities of the final result are multiplied by a factor of 10^9. Which is something, even in the huge search spaces we are discussing.

    That is the supposed role of NS.

    Now, let’s say that in the same population we have a number of possible neutral mutations in a certain time. And let’s say that in that time one drift event will expand one of those neutral mutations. Obviously, if one of the neutral mutations is “favorable” to the final result, and it is expanded by drift, in that case the probabilities of the final result will increase.

    But how likely is that scenario? Exactly as likely as a similar scenario for each of the other neutral mutations, that in no way contribute to the final result, or even make it impossible.

    IOWs. if we kust consider the pobabilities of a random walk from A to B (unrelated), all the states have similar probabilities of being reached, both with or without drift.

    That’s why I always say that drift is irrelevant to the computation of probabilities, and favours no specific configuration, least of all a functional one.

    Is that clear?

    Please, if you answer, be specific in your objections, so that I may respoind in a pertinent way.

  265. Elizabeth:

    Please, look at my post #50. It is meant for you too.

    And I would leave alone the problem of IC for the moment, and stick to the problem of origin of basci protein domains. The reason? Just to keep the discussion as focused as possible. We can discuss IC after, if you like.

  266. The “Father” of the Neutral Theory is none other than Motoo Kimura.

    Let me quote from his seminal work: “The Neutral Theory of Molecular Evolution”: p. 101

    In globins, as we have seen already, amino acid substitutions occur at the rate of about 10^-9 per amino acid site per year. This means that, roughly speaking, in the alpha-chain consisting of 141 amino acids, one substitution occurs on the average every 7 million years. Consider a mammalian species with an average generation span (g) of two years and comprising half a million individuals each generation (its effective population size may be much smaller). Let us suppose that the mutation rate, nu [Greek letter], per generation of alpha-globin is 10^-6. We restrict our consideration only to those mutations that cause amino acid changes. During 7 million years, the total number of alpha-globin mutation which occur in the species is then 2Nv x 7 x 10^6/g = 2 x (0.5 x 10
    ^6) x 10^-6 x7 x 10^6/2 = 3.5 x 10^6. Thus, 3.5 million mutations occur, among which only one becomes fixed. Not all of them are unique.

    7 million years, 3.5 million mutations, and only ONE is fixed.

    Is this supposed to explain evolution?

  267. I don’t know what you call it, PaV, and I don’t care very much; the important thing is that it’s a key part of modern evolutionary theory.

    Darwin didn’t even know what the source of variance in populations was, but what he noted was that if you have heritable variation in reproductive success, then the successful variants will become more prevalent.

    What we now know is that the vast majority of new variants are near-neutral, which means that any given population at any given time represents a pool of phenotypic variants of which some variants may prove more successful than others in surviving when the enviroment changes.

    This means that when we set up Darwinian computer models, we find, to our surprise, that complex functions evolve more readily than perhaps Darwin might have anticipated because necessary but neutral precursor variants are already likely to be there in the population.

    But let’s not trap ourselves into yet another categorical simplification: there aren’t three kinds of variant, deleterious, beneficial, and neutral. What there is is heritable variance in reproductive success. This means that (at least in sexually reproducing species) each generation will be a random sampling of the previous generation’s genetic makeup that is nonetheless biased in favour of those variants that tend to promote reproductive success in the current environment.

    You can call that whatever you like, but it’s fundamental to current evolutionary theory, and incorporates Darwin’s insight that he called “natural selection”, so it seems he earns his name on the tag.

    But what it does mean is that the old cliche that mutations are random and natural selection isn’t, is pretty well meaningless (and I wish people, especially Dawkins, would stop saying it!)

    Mutations and differential reproduction are stochastic process that are strongly biased in favour of what works.

    In that sense, they aren’t even “blind” or “undirected”. But I’m not going to argue about labels, because what matters is what the theory actually is, not the descriptive words we use to describe it.

    Evolutionary theory does not propose that evolution is “directed” in the sense that an ID proponent would use the term, i.e. planned by something with a distal goal that takes selected actions to achieve that goal. But it does propose that it is “directed” in the sense that a river is “directed” towards the sea, even though we cannot predict the course it will take, and the course it does take may be influenced by “random” events such geological changes to the landscape, and even factors caused by the river itself (hence meanders).

  268. It is this impotence of neutral drift that makes the neo-darwinian approach the only even remotely plausible explanation for the rise of protein domains.

    This is why gpuccio is using that model.

    I don’t see what’s so hard to understand here.

  269. What’s the big deal about fixation? Loads of highly prevalent alleles are not fixed. What matters is that there are loads of them.

  270. But how likely is that scenario?

    Apparently it is fairly likely, because it occurred in Lenski’s experiment, and Thornton seems to have found a historical example.

  271. Elizabeth, 23.3.1.1.7

    You completely missed the point of my post 23.3.1.1.6 (if you were replying to me). I specifically said in the last sentence:

    Note: I am not saying that this is ID, to just look at biology as see that it is obviously designed. I’m just pointing out the fallacy that is your made-up design-detection requirements of archaeologists.

    GinoB posted a fallacious representation of archaeological design detection, and I pointed out the obvious flaws in it. Of course if we find alien technology, we will immediately know its designed. Biological design is much tougher to scientifically decipher, because there IS a mechanism that can lead to adaptation. The problem there is that few outside of the ID camp seriously question the adequacy of neo-Darwinism to produce the “designs” at which we marvel in organisms. It was “100% adequate” around the turn of the 20th century when it was first adopted, and it has remained “100% adequate” every second since then through all of the challenges that should have been considered as we have observed more and more of the complexity. Every time we find a new level of complexity, the reaction is never “hmm, I wonder if the neo-Darwinian mechanism could have accomplished this”, it’s “Wow! This mechanism is even better than we thought! This genius design is highly selectable.”

  272. Petrushka:

    Briefly:

    a) In SCOP there are at present 110800 sequenced domains, grouped into 3902 families. In no case have we any evidence of bridges between those groupings. Do you really doubt that, even if that is certainly not the whole proteome, it is a significant sample of it? Have you any idea of how a statistical sampling is done? Are you saying that with 110800 sequenced domains we still have no idea pf the structure of the true proteome?

    b) Domain sequences do change in time through neutral mutations, with or without drift. But in most cases, they do retain hihly significant homology. How do you think that 1800 of those basci domains have been attributed to LUCA? Because, after almost 4 billion years, we still see homology between the proteins, say, in bacteria and humans.

    One example? If you blast the sequence of argynil trna synthetase in E. Coli and humans, a very old protein dating back to LUCA, you still get 232 identities out of 599 (39%), and 57% positives. The evalue is 1e-114. Well beyond any suspicion of randomness, I would say. And those proteins have diverged a lot of time ago.

    c) There were certanly extinctions. Who says they did not happen? Just explain why all the functional intermediaries between basic domains became extincted.

  273. Petrushka:

    Did Lenski’s experiment produce complex functional information? Or are you again passing microevolution for macroevoloution?

    What about Thornton? Reference, please.

  274. gpuccio, it seems to me you are attempting to carve nature other than at its joints! “Neutral drift”, “RV” and “NS” are not separable in the way you are trying to separate them, and “NS” does not have a “role” in any normal usage of the term. As so often, the metaphors are standing in the way of meaning.

    Both the generation of novel genetic variants and the effects those variants have on the reproductive success of the phenotype in the current environment are highly stochastic, but both are also biased in favour of what works.

    Most novel genetic variants will have little or no effect on the phenotype, and whether they do affect the phenotype, the effect may make absolutely no difference to the probability that the organism will reproduce successfully, in the current environment. This means, as you say, that the probability that a novel genetic variant will propagate through the population is a random walk, although the walk may be slightly biased. Imagine the classic drunk at a lamppost who staggers north and south down the street, the probability of going north or south at any one step being 50:50. Now imagine that there is a big cliff immediately south of the lamppost. Most drunks eventually will fall off the cliff, but quite a few of them will get quite a way northward before falling off, and some will even reach the temperance hostel at the far northern end, and be saved from the perils of drunkenness. If a variant is slightly beneficial, all you have to do is adjust your mental picture so that there is a gentle slope downwards to the north, so biasing the chances of the drunk ending up at the temperance hostel as opposed to off the cliff, and also increasing the number of drunks staggering about in the street.

    If it’s slightly deleterious, the reverse will be true – the street will slope slightly upwards to the North, and the cliff edge will claim more victims, and the temperance hostel fewer successes.

    But the really important point is that at any given time, there are lots of drunks in the street, so that if an environmental change comes along, so that the street changes slope, or even new streets appear at right angles to Main street, with slopes down them, there’s more chance that a drunk or two will find themselves somewhere interesting.

    And this is perfectly illustrated by the Lenski et al AVIDA paper, in which necessary steps to the beneficial steps were neutral, or even deleterious, yet they all evolved. They could not have done so unless neutral drift is reality, and the experiment showed (as have many others, as well as actual biological experiments) that it is indeed a reality. Indeed it is the reason why genetic diversity is so important to the survival of a population, and why small populations are in real danger even if there are substantial numbers of successfully breeding pairs. Variance is crucial to robustness, in many contexts.

    So let’s get back to basics, and lose these high-level terms like “NS” and “probabilistic resources” and “RV” and “drift” and figure out what evolutionary models actually propose. And for goodness’ sake, let’s stop using the word “random” without specifying exactly what we mean!

    We are dealing with probability distributions here, and those distributions are not flat!

  275. I don’t know whether it did or not, gpuccio, because I don’t know that anyone has attempted to measure it.

    But it seems to me that it produced functional information in normal usage (an algorithm emerged that could perform a function), and it was fairly complex (the genome of the function would have a very low probability of being generated by any process that did not incorporate differential reproductive success).

    And if you are going to distinguish between “microevolution” and “macroevolution” can you give the definitions you are using for those terms?

  276. Elizabeth:

    I am sorry, but I cannot follow you in that kind of “reasoning” (and believe me, I am being extemely generous here).

    You repeat “reproductive success” as a prayer or a mantra, and seem to believe that words will support your non arguments.

    “Neutral drift”, “RV” and “NS” are explicit concepts in explicit models. Dawkins knows that well. I know that well. You seem not to understand it.

    The Lenski and Avida things have nothing to do with dFSCI.

  277. Elizabeth:

    I have often given an explicit definition of dFSCI, and a personal threshold for biololgical dFSCI (150 bits).

    Most protein families analyzed by Dirston are wll beyond that threshold.

    Nor certainly Lenski or Avida.

  278. He doesn’t say that someone suspects it is an alien spacecraft, just that they suspect it is intelligently designed. Certainly, the debate about what the object is would immediately follow the identification of it being designed.

    The problem with interpreting living populations as designed is that we have a candidate for a natural process that produces incremental change over time.

    I agree! In fact I say as much in 23.3.1.1.9. Here is my comment:

    Biological design is much tougher to scientifically decipher, because there IS a mechanism that can lead to adaptation. The problem there is that few outside of the ID camp seriously question the adequacy of neo-Darwinism to produce the “designs” at which we marvel in organisms. It was “100% adequate” around the turn of the 20th century when it was first adopted, and it has remained “100% adequate” every second since then through all of the challenges that should have been considered as we have observed more and more of the complexity. Every time we find a new level of complexity, the reaction is never “hmm, I wonder if the neo-Darwinian mechanism could have accomplished this”, it’s “Wow! This mechanism is even better than we thought! This genius design is highly selectable.”

    Back to your post:

    We have no candidate for a designer capable of anticipating the results of sequence changes in DNA.

    And again, we don’t need a candidate. If we can objectively prove that an organic phenomenon is beyond the reach of random serach, natural law, or both (neo-Darwinism, that still leaves intelligence. Hypothetically, if one of Richard Lenski’s E. coli bacteria spawned with a completely re-written genome and hundreds of novel, complex functions, we would be 100% justified in rejecting neo-Darwinism. Would we be wrong to attribute it to design, at least until another mechanism could be proposed, because we don’t know who or what did it? Obviously we don’t have any such dramatic sweeping changes, so the debate is not that easy. But it just shows that you don’t need to even consider who the designer could be in order to conclude design.

    The large numbers cited as as evidence of design also make anticipation of genetic change impossible. there simply isn’t any way, even in principle, to anticipate changes in protein folding or regulatory sequences.

    For human intelligence, yes, that is virtually impossible. But you are disregarding the possibility that the designer’s intelligence could be many orders of magnitude, or infinitely, greater than our own. You have entered the realm of philosophy.

  279. GinoB:

    Common descent is a fact.

    Yes common descent as in I am descended from my human parents is a fact.

    ID is an unsupported hypothesis.

    ID is supported by scientific fields such as physics, biology, cosmology and chemistry.

  280. Elizabeth Liddle:

    That said, the evidence for Common Descent seems to me even more overwhelming than the pretty overwhelming evidence for Darwinian evolution as an explanation of Common Descent!

    Yet that same evidence can be used to support a common design.

  281. Well, have you tried calculating it for one of Lenski’s EQU outputs?

    And why did you set your “personal threshold” at 150 bits?

  282. Sure. Any evidence can be used to support a common design. That’s the problem.

  283. Where did that EQU come from? It sure as heck doesn’t represent any evolutionary reward from the real world.

  284. It evolved, Joseph.

  285. Wrong again, as usual.

    Only evidence of SIMILARITIES can support a common design- obviously you have absolutely no idea what a common design is and obvioulsy you have never dealt with IEEE nor building codes.

    Your ignorance is not a refutation.

  286. Yup just make stuff up…

  287. Ah. So your designer is incapable of making dissimilar organisms?

  288. No, I read the paper.

  289. Ahh so your only response is to act like a child?

    Have you even bothered to look around and observe how dissimilar organisms are?

  290. Read this:

    The effects of low-impact mutations in digital organisms
    Chase W. Nelson and John C. Sanford
    Theoretical Biology and Medical Modelling, 2011, 8:9 | doi:10.1186/1742-4682-8-9

    Abstract:
    Background: Avida is a computer program that performs evolution experiments with digital organisms. Previous work has used the program to study the evolutionary origin of complex features, namely logic operations, but has consistently used extremely large mutational fitness effects. The present study uses Avida to better understand the role of low-impact mutations in evolution.
    Results: When mutational fitness effects were approximately 0.075 or less, no new logic operations evolved, and those that had previously evolved were lost. When fitness effects were approximately 0.2, only half of the operations evolved, reflecting a threshold for selection breakdown. In contrast, when Avida’s default fitness effects were used, all operations routinely evolved to high frequencies and fitness increased by an average of 20 million in only 10,000 generations.
    Conclusions: Avidian organisms evolve new logic operations only when mutations producing them are assigned high-impact fitness effects. Furthermore, purifying selection cannot protect operations with low-impact benefits from mutational deterioration. These results suggest that selection breaks down for low-impact mutations below a certain fitness effect, the selection threshold. Experiments using biologically relevant parameter settings show the tendency for increasing genetic load to lead to loss of biological functionality. An understanding of such genetic deterioration is relevant to human disease, and may be applicable to the control of pathogens by use of lethal mutagenesis.

  291. Well, you have just made a differential prediction, Joseph, for which I commend you.

    I’m asking what evidence would refute ID. You seem to suggest that dissimilarities would refute ID.

    How dissimilar would things have to be to refute ID?

  292. I have already told you what would refute ID and very dissimilar organisms would only refute a common design.

    To refute ID- as Behe, Meyer, Dembski, Wells, et al., have said- all you have to do is demonstrate blind, undirected chemical processes can account for a living organism- Do that and there is no longer a requirement for a designer.

  293. No, I am not using “reproductive success” as a “mantra” gpuccio, I’m using it because it is a more direct description of what we are actually talking about when we talk about “NS” and “RV” and “neutral drift”.

    And my arguments are certainly not “non-arguments”!

    By “differential reproductive success” I simply mean what it says on the tin; that some organisms reproduce more successfully than others – produce more viable offspring. This may be due to luck, or it may be due to something they inherited from their parents, for instance, better camouflage.

    That is why “heritable variance in reproductive success” is a better name for “natural selection” because that’s all it is. Non-heritable variance in reproductive success would just be luck.

    If I’m spider and I produce few children because you wash me down the plug hole, then I’m not going to pass on “wash-down-the-plug-hole genes” to my offspring because there aren’t any. So while I may have less reproductive success than my peers, it isn’t heritable reproductive success (unless you washed me down the plug hole because I had particularly googly eyes, in which case, if that was a systematic effect, we might get cuter spiders after a while, but let that pass….) On the other hand if I don’t have many offspring because I am bright red and easy for predators to spot, whereas my peers are a dull green, and tend not to be eaten, then my genes for bright-redness will tend to fair worse in the population than my peers’ genes for dull greenness. On the other hand, if I have more children because my venom is more effective at killing juicy flies, then my venom genes are going to do better in the population than those of my less venomous peers.

    Not a mantra, then!

    “Neutral drift”, “RV” and “NS” are certainly concepts, but they are high level concepts, and only implemented in explicit models at the level I have given, i.e. at the level of differential reproductive success. Dawkins makes many errors with this. The reason I “don’t understand it” is because it doesn’t make a lot of sense. What I am saying is much simpler, and, IMO, makes much more sense. Indeed it’s exactly what AVIDA uses, and the result is evolution.

    Tell me why “the Lenski and Avida things have nothing to do with dFSCI” :)

  294. Ah, so your design inference depends on OOL?

    What was all that stuff about whales about, then?

  295. The design inference has ALWAYS been about the origin of living organisms- always.

    The stuff about whales is about evidence as in you need some that demonstrates the transformations required are possible via genetic variation.

  296. GinoB,

    The first step in identifying suspected design, and the most important step, is understanding the identity and capabilities of the designer.

    See my comment # 23.3.1.1.6 where I respond to these thoughts of yours. To archaeologists, of course the most important part of their process is identifying the designer(s), how it was made, what it was used for, etc., not whether or not it was designed. But you are simply lying that you say we need to know those things to tell if a discovered object was designed.

    That’s the big part IDists won’t own up to, because they know their Omnipotent God wouldn’t be allowed in science classes. So they keep playing the “it’s not about the designer” game, and science keeps just rolling its eyes.

    We don’t address the identity of the designer in this forum because a.) it is not central or even relevant to the ID hypothesis, regardless of your assertions and b.) identifying the designer scientifically does not seem to be possible given our current observable evidence.

    Contrarily, I believe the reason that you and others keep bringing it up is because you KNOW that once anything metaphysical is mentioned on our side, it will be crushed in science departments and in courts, and the merits of our arguments won’t even have to be addressed.

    You DON’T need to identify anything about the designer to infer design. You simply don’t. As I stated in comment 23.3.1.1.6, design identification in biology is much more difficult than its archaeological equivalent, because there is a natural process that can cause adaptation beyond the means of simple law and chance mechanisms. But one example of identifying an object as designed without addressing who the designer was or understanding their capabilities completely demolishes the nonsense you have been posting on this thread (and, I’m guessing, many others) on this subject.

  297. GinoB

    As for evolutionary processes being sufficient, this has been demonstrated to the satisfaction of the scientific community for over 100 years.

    I point out the same thing all of the time, even on this very thread. It is a black eye for natural evolution, IMO. It was accepted as fact decades before we even began to pry the lid off the complexity that ID advocates believe poses serious challenges to natural evolution, and we are still tumbling down the rabbit hole, waiting to hit the bottom. It was never seriously questioned, there was never serious skepticism on a community-wide level. You pointing out that it was an accepted fact long before the relevant challenges ever came up doesn’t sway me the way you intend. But maybe that’s just me. It seems like every few years, we uncover another order of magnitude of complexity, and we haven’t even begun to adequately explain exactly how some of the most complex phenomena arise (like human consciousness). Yet with each complexity revelation (or timeline reduction…we’ve witnessed highly complex evolutionary events in a matter of decades as opposed to the “deep time” that was preached for so many decades), the prevailing science community response has zero skepticism towards the theory, but joyful exclamation at the newly revealed power of natural evolution.

    There are literally thousands of colleges, universities, natural history museums, and millions of pages of on-line text where you can learn about the evidence. People spend their whole lives studying and getting PhDs and only touch on a tiny portion of it. There’s far too much of it to give it adequate coverage here on this tiny blog. Get thee to a library!

    I have been actively seeking evidence rebutting ID theory since I came across the concept 7 years ago. I have asked many skeptics for references to such evidence, as have dozens of others on forums like this. I have yet to see one remotely successful paper or piece of evidence. The vast majority are evidence for common descent, “microevolution” or some other seemingly related yet actually irrelevant information.

    I honestly try to be as open-minded with any argument anyone makes on this issue. I would be lying if I said that I successfully do that all of the time or that it is easy; everyone comes to this table with a bias – everyone. But I do try to comprehend and rationally judge (for my own belief) the validity of any claim someone makes (unless they are being nasty). If I found convincing evidence that natural evolution is categorically capable of producing the complexity we find in life, I would have no huge problem abandoning ID. But arguments from authority like “everyone who matters believes it” or Elizabeth’s question-begging, simplistic argument;

    “…by the simple logical fact that if things replicate with heritable variation, and at least some of that variation is variation in reproductive success, the population will adapt to its environment”

    are not going to convince me that said replication with heritable variation in reproductive success can and did create the astounding biological complexity we have so far discovered and have yet to comprehend.

  298. Elizabeth:

    Well, have you tried calculating it for one of Lenski’s EQU outputs?

    No, because frankly I am not interested in GAs, that IMO are only examples of intelligent design.

    For dFSCI computation, you need a purely random system, or you have to isolate the random part of a complex algorithm.

    And why did you set your “personal threshold” at 150 bits?

    Empirical reasons. The 500 bit threshold of Dembski is an universal probability bound. It takes into consideration all the possible probability resources of the whole universe, from the big bamg to now, and at the level of elementary quantum particles and quantum times.

    That is frankly too much for a plaen of 4 billion years of existence, and for a maximum random system that has biological proportions.

    I simply tried to grossly compute the probabilistic resources of the whole planet, from the beginning of its existence, assuming that it was from the beginning covered by a bacterial population, and assuming a mean time of bacterial reproduction and a mean rate of mutations.

    I could not redo the calculation now without some research, but at the time I came out with a generous threshold of 150 bits.

    It’s just a proposal, I am ready to review the calculation if anyone has better data or better assumptions.

    But the 500 bits of Dembski’s UPB are certainly too much for a planetary biological system. I am tired of being too generous with darwinists!

  299. DrBot:

    I apologize if I am responding only now to your 46.2.1.1.3.

    The point you raise is interesting, but not pertinent to the discussion we were having.

    I wil be more clear.

    You say:

    One problem there is it is only comparing protein coding sequences. To get a full picture of the degree of isolation between domains you need to look at non-coding sequences as well because these can potentially provide routes between domains.

    The point is: we were discussing transition through selectable intermediates.

    While the role of non coding DNA is certainly interesting (more on that later), one thing it cannot do is provide selectable protein intermediates. That’s, indeed, exactly because it is “non coding”.

    Non coding DNA is not translated, by definition. Therefore, it does not produce a protein. A proteins that is not produced cannot obviously give a reproductive advantage, abd therefore be selected by NS.

    Beware: mutations in non coding DNA can certainly give a reproductive advantage abd be selected, but not certainly for their protein coding information. So, I can’t see how non coding DNA can represent a bridge between protein coding domains, if it does not code for a translated protein.

    On the other hand, I am indeed a big fan of non coding DNA. I do believe that new genes can emerge from non coding DNA, but certainly not by darwinian mechanism.

    Transposons have been considered an import tool in modifying DNA, including non coding. I agree with that.

    The point is, before a segment of non coding DNA generates an ORF, it is not translated, Therefore, no protein related information in it can ever be selected. So, if new genes emerge (as I believe) form non coding DNA, for example by transposon activity, there are only two possible explanations:

    a) Pure random variation, with no NS

    b) Design

    Guess my choice?

  300. Thanks for the response,

    The point is: we were discussing transition through selectable intermediates.

    The problem is you are assuming that intermediates have to be selected for. They don’t, they can just be near neutral. This, I would argue, is a fundamental misunderstanding you have of evolutionary processes.

    Non coding DNA is not translated, by definition. Therefore, it does not produce a protein. A proteins that is not produced cannot obviously give a reproductive advantage, abd therefore be selected by NS.

    Again, they don’t need to confer a reproductive advantage, just not a severe reproductive disadvantage.

    Think of it this way – if a protein coding gene can mutate into a psuedogene, then a psuedogene can mutate into a protein coding gene. Now what else can a psuedogene mutate into, and what else can mutate into a psuedogene?

    To put it another way – if we are discussing, metaphorically, how to get from rock A to rock B, you appear to me to be arguing that there is no way to get from A to B because we know of no rocks in between. I am saying that there is more to the terrain (the genes) than just rocks (protein coding genes) and that some of the non-rock terrain may be relatively flat (neutral), providing routes to other rocks.

  301. by the same logic…

    There are about 142,000 characters in Hamlet. I make a program that randomly generates 1,000,000 characters per second. I’ll recreate Hamlet in no time!!

    No, I didn’t mention selection, but neither did you. …Unless you’re suggesting that 150 mutations per generation were selected. That is fantastically generous considering that those mutations had to “stumble” towards human consciousness, among other things.

  302. GinoB

    But the combined iterative process of RV filtered by NS with entities that retain heritable variations can and does easily create new features and complexity.

    You’ve only had that explained to you several dozen times by now.

    Actually we have had it asserted several thousand times on this site and in other forums. Demonstrated or proven? Still waiting on the first one.

    Mutation + selection “easily” stumbled upon human consciousness in a few hundred thousand generations?

  303. uoflcard

    GB: “But the combined iterative process of RV filtered by NS with entities that retain heritable variations can and does easily create new features and complexity.

    You’ve only had that explained to you several dozen times by now.”

    Actually we have had it asserted several thousand times on this site and in other forums. Demonstrated or proven? Still waiting on the first one.

    It’s demonstrated every time a genetic algorithm is used to produce a completely new complex design with an iterative process that follows a few simple rules. One quick example:

    Automated Analog Circuit Design Using Genetic Algorithms

    The process is identical to what happens in the reproduction of biological life. There is more than one way to achieve complexity beside just designed and manufactured complex from the start. Iterative filtered feedback processes can do it too.

    Complexity by itself is not a sure indication of one-time design

    Mutation + selection “easily” stumbled upon human consciousness in a few hundred thousand generations?

    ‘Consciousness’ has almost certainly been around for a lot longer than that. ‘Human consciousness’ only since the time you define in our evolutionary timeline as the appearance of first humans.

  304. 304

    I’ve been stuck unable to comment for a few days, and this has really irked me.

    What selects for Mozart’s brain? Or ours? How does Dawkins’ indifferent universe a.k.a. law of the jungle produce pleasantly enlightening musical entertainment?

    Of course you’ll say that it’s an anomaly, like a water-skiing dog. Fine.

    What about the average human intellect which none of us use? Every other case in which a feature goes unused it is considered vestigial. What about the brain?

    Are we supposed to believe that at some point in prehistory our distant ancestors were forced to learn multiple languages and calculus and engineering and whatever else was thrown at them, in excess of anything any modern man has ever comprehended, all in order to survive?

    I’ve heard ridiculous sexual selection story. So let me rephrase. Was there ever a time in prehistory when our distant ancestors had to do all the above things in order to get a mate?

    It’s the equivalent of saying that giraffes needed longer necks to reach the tops of trees, and that’s why they are 4,000 feet long.

    The existence of the human intellect falsifies Darwinism.

    Any evolutionary narrative requires an extended period during which survival or reproduction required the entire lineage to exercise a mental faculty surpassing the greatest minds in history. And while leaving a deceptive trail indicating the a gradual development of language, writing, and technology with our present state as its pinnacle.

    Which does evolution predict – vast, untapped capability or whichever characteristics are required for survival, allowing for a degree of fluctuation?

    Doesn’t evolution predict that our minds should never happen? Why doesn’t it predict that?

  305. 305

    Let me rephrase this as an evolutionary prediction.

    Evolutionary theory predicts that living things should possess features or behaviors that are necessary for their survival or reproduction, or were at some point necessary for the survival or reproduction of their ancestors.

    Is that an accurate prediction of evolutionary theory?

  306. It’s demonstrated every time a genetic algorithm is used to produce a completely new complex design with an iterative process that follows a few simple rules. One quick example:

    Automated Analog Circuit Design Using Genetic Algorithms

    The process is identical to what happens in the reproduction of biological life. There is more than one way to achieve complexity beside just designed and manufactured complex from the start. Iterative filtered feedback processes can do it too.

    I cannot speak about the paper you linked by Navid Azizi, but I will look at it as soon as I can. Recently, I have spent time looking at Avida, specifically the 2003 Nature paper by Richard Lenski et al, The evolutionary origin of complex features. I am still new to genetic algorithms, but I have some serious initial doubts about Avida regarding its analogy to biological evolution. Biological mutations are random with respect to fitness or function, but mutations in Avida, while random wrt the rewardable outputs, are randomly inserted from one of 26 functions…every insertion is an actual funciton. That is nothing like what we should expect in biology.

    Even though I haven’t read the Azizi paper, I am initially very skeptical of your claim of it being “identical” to the reproduction of biological life. You were criticizing the use of “superficial similarities”, like the flagella vs. outboard motors, in this very thread at comment # 23.3.1.1.4 (emphasis added):

    The way archaeologists determine if a find is human produced (say a primitive stone ax) or just a natural rock is by comparing the object with other known human designed similar objects. Not superficial similarities, not analogies (like flagella and outboard motors) but actual known designed objects.

    Every genetic algorithm that I’ve seen has claimed to be “proof” of Darwinian-like mechanism creating complex functionality has one huge assumption/aide built into every one of them: a smoothly sloped function gradient. Weasel was the most ridiculous example, of course, but even Avida does this… they nine (9) incrementally complex functions that build towards the final desired function (EQU), and they are rewarded exponentially greater and greater. Most ID advocates will admit that the neo-Darwinian mechanism is capable of creating complex functionality when each step forward is small enough to be traversed by random search. as gpuccio said in #38:

    RV + NS in principle could, but only if the pathway to the complex information could be deconstructed into steps of low enough functional complexity…

    This is all Avida demonstrated. In fact in the Discussion section, the authors stated:

    The most complex function, EQU, evolved only when several simpler functions were also useful.

    and

    Some readers might suggest that we ‘stacked the deck’ by studying the evolution of a complex feature that could be built on simpler functions that were also useful. However, that is precisely what evolutionary theory requires, and indeed, our experiments showed that the complex feature never evolved when simpler functions were not rewarded.

    i.e. they proved nothing other than what everyone agrees on, that RM+NS can create ANYTHING…that has a smooth enough fitness gradient leading up to it. And this gradient was constructed by the programmers of Avida, so what’s the point? btw, here is there “reward curve” for output functions (the number is the “computational merit”, analogous to the “fitness value” it adds to the organism):

    NOT – 2
    NAND – 2
    AND – 4
    OR_N – 4
    OR – 8
    AND_N – 8
    NOR – 16
    XOR – 16
    EQU – 32

    It is Table 1 of their paper, which I linked above.

  307. DrBot:

    Again with neutral mutations. I have explained. If you don’t understand, what can I do?

    So, to sum up: do you belioeve that the transitions from one existinf basci domain to a new one happened without selectable intermediaries? That my assumption that there must be selectable intermediary, expanded selectable intermediaries, and a lot of them, is only “a misunderstanding I have of evolutionary processes”?

    OK, it’s fine for me. You are the first darwinist I know who believes in evolution by RV alone.

    Then, it’s mud to Mozart by chance alone, all the way.

    Congratulations: you have just refuted the neo darwinian model, cancelled NS form the scenario, and proposed the most blatantly absurd explanatory theory for the origin of protein domains.

  308. gpuccio, I have to say that from where I’m standing it really does look as though you are misunderstanding what DrBot and I are saying.

    Please consider that your separation of “RV” “NS” and “neutral drift” are not very useful way of parsing evolutionary theory!

    Neither of us think that “RV alone” produces evolution. “RV alone” is a pretty useless concept. What do you mean by “RV alone”? Variants with no phenotypic effects at all? Or variants with completely neutral phenotypic effects under all environmental conditions?

    Is your argument that precursor sequences of new protein domains must be neutral, and there must be too many of them to be probable?

    In which case, how are you computing that probability?

  309. It’s scarcely a prediction, ScottAndrews – we know that they do. It’s what requires explanation. Evolutionary theory is one explanation.

    A prediction of evolutionary theory is that we should see incremental adaptations in the direction of an optimum along each lineage.

  310. 310

    Elizabeth,

    I should have included one more word:

    Evolutionary theory predicts that living things should possess only features or behaviors that are necessary for their survival or reproduction, or were at some point necessary for the survival or reproduction of their ancestors.

    For example, if giant peacock feathers are explained as a result of reproductive selection, then for the sake of argument, fine. But you should never find a predator that can run 100mph for ten minutes if the fastest prey animal can run 20mph for 1 minute.

    With the addition of “only,” should that not be a prediction of evolution? I assert that it must be.

  311. Elizabeth:

    But… Have you followed the discussion between me and DrBot?

    It’s DrBot, not me, that refuses NS in the reasoning.

    My reasoning was simple: if NS helped in the formation of new domains, we should have expanded (selected) functional intermediaries. And it seems that strangely all of them have disappeared.

    Simple, isn’t it?

    But no, nothing is simple with darwinists. So DrBot objects:
    “The problem is you are assuming that intermediates have to be selected for. They don’t, they can just be near neutral. This, I would argue, is a fundamental misunderstanding you have of evolutionary processes.”

    ???? I have never “assumed that intermediates have to be selected for”.

    I am assuming nothing.

    I am saying:

    a) If intermediates are not functional, and are not selected, they don’t help in comparison to simple random variation. In that case, the system is acting randomly, there is no selection, no amplification. Accidenmtal amplification may occur by drift, but, as already discussed, that cannot favour any functional result, and is still pure random variation.

    Well, I am not saying that “intermediates have to be selected for”. I an saying that, if they are nor selected for (they are neutral or quasi neutral), they are of no special utility to the explanation of the result.

    It’s not the same thing.

    b) If, instead, intermediates are functional, and are selected for and amplified, then the algorithm is surely much more powerful, and many probabilistic walls can be overcome.

    But we should find the intermediates, ot at least some of them.

    You ask:

    Is your argument that precursor sequences of new protein domains must be neutral, and there must be too many of them to be probable?

    No, as you can see. My argument is that according to what we observe, the best explanation is that those functional precursors did not exist. Because otherwise we would have trace of them.

    So, for purely empirical reasons, we should get rid of the hygpothesis that there were many functional precursors, selected and then erased. It just does not work. It is falsified by what we can observe.

    Obviously, it is always possible that domains evolved by neitral evolution, and in that case it is less suprising that the precursors are not found (well, if they were amplified by drift, we should find them just the same, but whatever…).

    The problem is, if the systen is only random, or mainly random, the probabilities are those relative to the whole dFSCI of each protein. So, just to reason according to the results of the Durston paper, mosat protein families are well beyond the threshold of “credibility” I have suggested (150 bits). Well, many of them are also beyond Dembski’s UPB of 500 bits.

    You ask:

    “how are you computing that probability?”

    Whow! Must I start all the discussion about dFSCI and the design inference again?

  312. No, it isn’t, because of drift effects.

    Scott, it’s been nice talking to you, but I think it’s time I left you guys to yourselves :)]

    If you want to get in touch, I’m here:

    http://theskepticalzone.com/wp/

    and you, and everyone else, are very welcome to drop by. The idea behind the site is that it is a place where people with very different views can debate with as little rancour as possible. At least, that’s the idea :)

    Hope to see you around.

    Lizzie

  313. 313

    Elizabeth,

    I’ll reply anyway.

    When you say “drift,” you seem to mean “current.” Why does your idea of drift work like a current?

    Why would drift, which doesn’t even pretend to act systematically, incline toward greater and greater unneeded capability?

    If this is what drift does, even occasionally, then where are the other examples besides human intellect? Where are the cheetahs that can run 100mpg but never do because their prey never runs that fast? Where are the birds that can ascend out of the atmosphere but never do because there’s no reason to go there?

    How can you use drift to explain the “normal” variation and also use it to explain the bizarre anomaly? Is there anything that drift can’t do?

  314. Again with neutral mutations. I have explained. If you don’t understand, what can I do?

    Listen and try and understand – perhaps read some textbooks on evolutionary theory ;)

    OK, it’s fine for me. You are the first darwinist I know who believes in evolution by RV alone.

    Clearly you haven’t been reading my posts for comprehension.

    Congratulations: you have just refuted the neo darwinian model, cancelled NS form the scenario, and proposed the most blatantly absurd explanatory theory for the origin of protein domains.

    Again, making up a ridiculous position, claiming that I hold that position, then knocking it down with sarcasm is not really very impressive.

    My reasoning was simple: if NS helped in the formation of new domains, we should have expanded (selected) functional intermediaries. And it seems that strangely all of them have disappeared.

    NS acts on the phenotype – if an organism is born with one genotypic trait that gives a reproductive advantage, and one or more traits that diverge from the parent(s) but do not influence reproductive succes then those neutral traits are, in a sense, being selected for, because they contribute to a phenotype that is sucesful.

    Well, I am not saying that “intermediates have to be selected for”. I an saying that, if they are nor selected for (they are neutral or quasi neutral), they are of no special utility to the explanation of the result.

    Well see my response above – your mistake seems to be in considering genes in isolation and not in the contect of the genotype and phenotype. Neutrality increases the effectiveness of search in large dimensional search spaces – there is a lot of literature out there on neutrality and fitness landscapes – if you ignore, or fail to understand the effects then your probability calculations will always be wrong.

    If, instead, intermediates are functional, and are selected for and amplified, then the algorithm is surely much more powerful, and many probabilistic walls can be overcome.

    But we should find the intermediates, ot at least some of them.

    Yes, if there is a path up a fitness landscape from A to B then it is the easiest route to find. Fitness landscapes that have lots of neutrality provide many routes from A to B, not just up hill ones.

    I agree that there should be some intermediates – what would they look like? Psuedogenes, non-coding regions … ?

    “how are you computing that probability?”

    Whow! Must I start all the discussion about dFSCI and the design inference again?

    You could start by explaining why you discount from your probability calculations things that affects the probability?

  315. The problem is, if the systen is only random, or mainly random, the probabilities are those relative to the whole dFSCI of each protein.

    Evolutionary search is not the same as random search, it only searches locally. Drift is a part of that search – that’s why it is called drift and not random jumping – genotypes drift along neutral parts of the landscape.

    From the perspective of proteins, drifting can involve ANY gene sequence, not just protein coding ones, just so long as it has a near neutral effect on the phenotype. When you look at the probabilities you have to take into account potential pathways across the whole gene space – any route that is viable can potentially be taken – and consequently intermediates between different protein domains can potentially be any type of gene that does not have a detrimental effect on the phenotype.

  316. DrBot: “So in one case you have a thing that eternally exists, and causes the universe to exist, and in the other case you have a thing that eternally exists, and causes the universe to exist. But in one of those two cases there is an absurdity of an infinite regress of causes …

    Can you explain why?”

    Sorry for the late response.

    Yes. I’m going to assume that you are familiar with what is meant by an infinite regress of causes.

    It becomes an absurdity only if we are dealing with causes that require material existence.

    It is not an absurdity if the first cause of all that contingently exists is outside of material reality.

    Something or someone could have caused everything that began to exist. That something or someone could not itself or him/herself be a part of that which was caused, because then he/she/it would enter into the realm of the absurdity. Actual infinites in space and time are logically untenable. There’s more on why this is so, but for the sake of brevity I’ll leave that one alone for now.

  317. Elizabeth (emphasis added):

    But what it does mean is that the old cliche that mutations are random and natural selection isn’t, is pretty well meaningless (and I wish people, especially Dawkins, would stop saying it!)

    Mutations, and differential reproduction are stochastic process that are strongly biased in favour of what works.

    In that sense, they aren’t even “blind” or “undirected”. But I’m not going to argue about labels, because what matters is what the theory actually is, not the descriptive words we use to describe it.

    I admittedly do not understand your argument here, specifically the bold part. How can natural mutations be biased in favor of what works? If you mean that they originate in a biased manner, I see how that applies to a natural modern synthesis. If you mean that they propogate in a biased manner, to me that means that natural selection behaves in a biased manner. Either way, I don’t understand your point or why you feel it is important to state it. Further explanation?

  318. DrBot:

    I had already addressed those points in my post #50 (to you).

    I quote myself:

    “DrBot:

    Let’s try some order.

    Look at my post 38.1.1:

    “And it is well obvious, even if the dumb logic of darwinists will never recognize it, that neutral mutations in no way change the probabilities of a random walk, and neither does genetic drift, because it is a purely random event, and therefore does not change anything. The term “RV” includes all forms of possible random variations, including neutral mutations and genetic drift. And all RV is accounted for and evaluated in the ID model.”

    and my post 47 (in response to you):

    “IOWs, the point is:

    a) We have a domain that appears for the first time (B).

    b) To explain that by neodarwinian mechanisms, we need some precursor (A), previously existing, that by RV and NS gave the result of the appearance of B. The only alternative would be that the transition from A to B was merely by RV, that is neutral mutations and drift and similar. But, as both A and B are unrelated long molecules, that is practically impossible: the probabilities are completely against that, and any good neodarwinist knows that.”

    And so on.

    Some more reflections on the reason why drift is non relevant in the computation of probabilistic resources.

    Now, let’s say that in the same population we have a number of possible neutral mutations in a certain time. And let’s say that in that time one drift event will expand one of those neutral mutations. Obviously, if one of the neutral mutations is “favorable” to the final result, and it is expanded by drift, in that case the probabilities of the final result will increase.

    But how likely is that scenario? Exactly as likely as a similar scenario for each of the other neutral mutations, that in no way contribute to the final result, or even make it impossible.

    IOWs, if we must consider the pobabilities of a random walk from A to B (unrelated), all the states have similar probabilities of being reached, both with or without drift.

    That’s why I always say that drift is irrelevant to the computation of probabilities, and favours no specific configuration, least of all a functional one.”

    So, let’s sum up (maybe for the fifth time to you):

    The propblem with the transition from one to another complex unrelated state (unrelated means that they share no significant sequence homology, like all basic protein domains), then:

    a) the search is not local. It is a random walk that has to necessarily traverse the space

    b) it is perfectly possible to traverse the space, thorugh neutral mutations and other kinds of variation (some of which, like frameshift mutations, can provide immediate jumps). But the probabilities of reaching a specific unrelated state through RV are extremely low, if the search space if big.

    IOWs, if there are 10^150 unrelated non functional states, and only 10^10 unrelated functional states, the probability of reaching an unrelated functional state if 1:10^140.

    That means that, any time you reach an unrelated state through a random walk, by neutral mutations, drift, frameshift mutation, inversion, translocation, ot whatever, the probabilities that such a state is functional are 1:10^140.

    Not good, eh?

    Genetic drift, or the possibility you siggest that neutral m utation are expanded “together with” a selected mutation, do not alter this situation at all. The rate between functional and non functional unrelated states remains the same.

    Therefore, I don’t understand for what sirt of mental hypnosis you go on stating, with admirable stubborness, that neutral mutations and drift and so on change the probabilites.

    It’s nonsense. It’s wrong. Try to motivate it, or remain silent. Anyway, I will not explain the same things for the nth time.

  319. Elizabeth (emphasis added):

    But what it does mean is that the old cliche that mutations are random and natural selection isn’t, is pretty well meaningless (and I wish people, especially Dawkins, would stop saying it!)

    Mutations and differential reproduction are stochastic process that are strongly biased in favour of what works.

    In that sense, they aren’t even “blind” or “undirected”. But I’m not going to argue about labels, because what matters is what the theory actually is, not the descriptive words we use to describe it.

    I admittedly do not understand your argument here, specifically the bold part. How can natural mutations be biased in favor of what works? If you mean that they originate in a biased manner, I see how that applies to a natural modern synthesis. If you mean that they propogate in a biased manner, to me that means that natural selection behaves in a biased manner. Either way, I don’t understand your point or why you feel it is important to state it. Further explanation?

    OK, apologies, let me try to make it clearer what I mean:

    By “mutations” I mean novel sequences in the genome (sequences present in neither parent). Near-neutral mutations are far commoner than strongly beneficial or strongly deleterious mutations, and include mutations that have no phenotypic effect at all, as well as those that have a phenotypic effect that makes no difference at all to reproductive success. In that sense, even before we consider the filtering effect of differential reproduction, the actual generation of variants is biased in favour of what works, i.e. something that is similar to the sequence present in what is by definition a viable parent.

    This in itself is a potential outcome of Darwinian processes, in that organisms with reasonably hi-fidelity reproduction mechanisms will tend to leave more copies of their genome around than organisms with low-fidelity reproduction mechanisms.

    I am not saying that variant-producing mechanisms are biased in favour of what works better, merely in favour of what works about as well as the parent genotype. It’s a highly non-flat probability distribution, in other words, with a peak around neutral.

    Hope that makes a little more sense :)

    Will drop by again to check.

  320. Still going to extract myself for a bit, but on reflection, I’ll try and respond to posts addressed to me!

    I just try not to be distracted by new shiny things!

    No, I don’t mean “current”. A “current” would be analogous to something that is biased towards or away from propagation, because it promotes or undermines reproductive success. “Drift” is the name we give to what happens to variants that are neutral in the current (no pun intended) environment, and are therefore as likely to be slightly less prevalent as slightly more prevalent in each successive generation. A random walk in other words.

    And “drift” doesn’t “do” anything, other than be the word we give the phenomenon by which populations are continually enriched with neutral variance. The reason that is important is that if the environment changes, that neutral variance can be potentially beneficial, and by “environment”, I mean not only the external environment, which includes the population itself, and its ever-changing allele frequencies (gene *environment interactions), but also the “genetic environment” – a variant that is entirely neutral in one genotype may be beneficial in another (gene * gene interactions)

    So I hope it is now clearer what I mean by drift. Like “selection” it isn’t an agent, it’s just an observed phenomenon, but it’s important, because it means that genetic diversity, which enables populations to adapt to changing environments, consists of a gene pool of variants including those that were originally neutral, not merely variants that were beneficial from the get go.

  321. Elizabeth:

    So, let’s sum up, another time:

    a) Neutral mutations are not in any way tending to a new function (your words: “I am not saying that variant-producing mechanisms are biased in favour of what works better,”

    b) They must be neutral, not to be exposed to negative selection, in which case they would reproduce worse (your words: “merely in favour of what works about as well as the parent genotype.”

    c) And yet, new biological functions appear all the time in the course of natural history, under the form of new basic protein domains that accomplish new things.

    e) How do we explain that? If we invoke NS, then we are no more relying on neutral mutations only. But against a significant role of NS there are at least two big empirical facts:

    e1) The complex biochemical functions of basic protein domains are not decontructable into simpler progressive steps with naturally selectable functions, not even in one case, least of all in the general case.

    e2) No trace of any intermediate sequence “bridging” basic protein domains is found in the proteome.

    I have explained in detail, many times, why neither e1 nor e2 can be answered from a NS point of view. Nobody has given any concrete counter argument, only evasion, usually again in the direction of neutral selection and drift, which are not pertinent in this specific discussion (remember, this is point “e)” that starts with “If we invoke NS, then we are no more relying on neutral mutations only.”

    f) If, instead, we leave alone NS, or at least drastically redefine its role to solve our problems in e), then we are faced by another problem: probabilities.

    g) You know very well that RV favours local searches. You have said that yourself, suggesting that that would be a reason not to rely on a uniform distribution in the computation of probabilities. But that is simply worng. Local searches are not useful here. Local searches can, at best, tweak an existing domain, or slightly change an active site. But to produce a new domain, unrelated, at the sequence level, to anything that already exists, we have to abandon the local. The local is the set os sequences with high homology to what exists.

    h) Once we abandon the local, and dive into the sea of unrelated states, the distribution of probabilities becomes practically uniform: each unrelated state has more or less the same probabilities to be reached by a random walk.

    i) The sea of unrelated states is extremely huge for most (almost all, indeed) known functional protein domains (see the discussions on dFSCI and the Durston paper).

    l) As a consequence, functional basic protein domains are the perfect objects to infer design: they exhibit lots of dFSCI, their origin by a pure random system (neutral mutations and genetic drift) is practically impossible, and the only explicit mixed algorithm (RV + NS, the neodarwinian algorithm) is falsified by existing evidence (see points e1 and e2).

    That’s my reasoning. I have made it as simple and schematic as possible.

    Now, please, don’t argue again that I should not talk of NS and RV, but rather of differential reproduction of inheritable traits, or whatever. Don’t insult my intelligence, and especially yours.

    If you have objections, please take my points, my terms, and my reasoning, and say explicitly where and why they are wrong.

  322. Elizabeth:

    Just another note: drift does not “enrich” anything. If a neutral mutation es expanded by drift, other neutral mutations are lost in that expansion. There is no enrichment. Drift is absolutely useless, or at least it does nothing different from what other kinds of RV do: it randomly changes the existing sequences.

    We cannot even say that drifts accelerates the rate of variation. First of all it is a rare event. Other forms of variation are much more common.

    Secondly, we know well that too much variation is worse than too little. That is well known, I believe, in population genetics. You cannot increase your chances of reaching new functional targets only by increasing the rate of variation, be it by drift, or by any other means.

    Just an example of how drift can be in the same way useful or deleterious, so that its global effect is nil.

    Let’s say that to reach B you need serine at position 126. Well, you get lucky enough and get that mutation in A. It is not amlified, but luckily it is neutral, so it is not lost too. It is there, ready to contribute to the final result (provided that other lucky events accumulate).

    Now, if by further luch that neutral mutation is expanded by drift, we will certainly be nearer to the goal.

    But in the population there are many other neutral mutations. After all, as you say, neutral mutations don’t tend to favour what works better.

    Now, let’s say that for once you are not lucky, and the neutral mutation that is expanded by drift is one, in another individual, that has glycine at position 126. Now, that is a neutral mutation for A, but it is not neutral at all for the future target, B. Indeed, let’s say that with glycine at 126, B will never be functional.

    Now, if the neutral glycine is expanded by drift, instead of the neutral serine (they have the same probability, after all), what has happened? You have lost the favourable neutral mutation that had already accumulated.

    That is the truth for neutral mutations and genetic drift. They don’t change the explanatory scenario.

    The only place where they are “useful” are the wrong arguments of darwinists.

  323. No trace of any intermediate sequence “bridging” basic protein domains is found in the proteome.

    That is just a hidden version of why are there no intermediates among contemporary organisms.

    why should there be?

  324. 324

    Petrushka,

    That is just a hidden version of why are there no intermediates among contemporary organisms.

    Wow. The lack of evidence to support one speculation provides an explanation of the lack of evidence to support yet another. Evidence is evidence, and no evidence demonstrates consistency with other cases in which there is no evidence.

    You’ve got all the bases covered. This can never be wrong.

  325. Lizzie:

    Sorry for taking so long to reply. I must admit that with this new format, and with the sheer number of posts taking place each day, it’s very hard to keep track of where I’ve left an entry. (Hope somebody’s taking note) But, I’v also been away from a computer for a couple of days.

    Now,

    I don’t know what you call it, PaV, and I don’t care very much; the important thing is that it’s a key part of modern evolutionary theory.

    Certainly neutral drift is part of “modern evolutionary theory”; however, it has serious problems—which you seem to deny for whatever reason. But let’s move on.

    What we now know is that the vast majority of new variants are near-neutral, which means that any given population at any given time represents a pool of phenotypic variants of which some variants may prove more successful than others in surviving when the enviroment changes.

    This is probably true—given enough time for drift to work. But, is the mere ‘presence’ of such ‘successful variants’ sufficient. Obviously the ‘presence’ of these putative ‘successful variants’ is necessary. But is it also sufficient for macroevolution to take place? We continue . . . .

    This means that when we set up Darwinian computer models, we find, to our surprise, that complex functions evolve more readily than perhaps Darwin might have anticipated because necessary but neutral precursor variants are already likely to be there in the population.

    Is this true? Do ‘Darwinian computer models’ actually show this? Behe and Snoke set up what they considered to be a ‘Darwinian computer model’ and they got no such result—in fact, it showed even NS, let alone neutral drift, was rather impotent to bring about meaningful changes.

    But let’s say that what you say is true. Well, what you’re saying is that the “necessary” neutral precursor (variant) is already likely there. Okay. But, as I said above, the variants are necessary, but are they sufficient to explain evolutionary change?

    This is where the whole idea of “fixation” comes in. You’re simply assuming that because this ‘beneficial’ (I know, ‘beneficial’ relative to the ‘current’ environment) is there, the rest automatically takes care of itself. But this is where, IMHO, you’re going wrong. The next step—which is ‘necessary’ and ‘sufficient’—is for this ‘beneficial variant’ to become fixed, wherein, every member of the population shares this variant.

    This is because, let’s say, a little kitten, born with a ‘variant’ that allows it to sniff out potential prey better than any of the other cats around, has a likely reproductive advantage over its litter mates as an adult. And so, too, would its offspring. But what if, one day, while still a kitten, it became distracted while crossing the street, and was run over. What, then, of this ‘beneficial variant’? What becomes of it? ANS: Nothing. It’s lost to the population.

    This is a random event, and this randomness—that is, the potential for a single member of the population to be accidently lost, or, for whatever reason, not be able to furnish offspring; or for the offspring themselves to be killed off or reduced in number—all these random kind of events need to be overcome by the population. And that’s why population geneticists calculate such things as “fixation” times. Once a variant is incorporated into the entire population, it’s very likely not to be lost very easily. And now the population, as a whole, can work on acquiring—and fixing!—the next variant. But how long does this take?

    Well, Kimura did the calculations, and it turns out to be 1/4N_eff. And, hence, in 49.1 below, I include a sample calculation from Kimura’s magnus opus, “The Neutral Theory of Molecular Evolution”. It turns out that this is a very slow process.

    So……the mere appearance of a ‘beneficial variant’, though ‘necessary’, is not sufficient. Fixation is also a necessary, and somewhat sufficient condition for macroevolution to occur. The problem though is that this “fixation” process works way too slowly to account for the fossil record. This is only more so the problem when considering chimp—human differences (only 4 million years for all these “fixations” to occur!)

    But what it does mean is that the old cliche that mutations are random and natural selection isn’t, is pretty well meaningless (and I wish people, especially Dawkins, would stop saying it!)

    Dawkins is the leading apologist for the Darwinian cause. His entire argument falls apart if NS is considered to be ‘random’. Per your view, his arguments fall apart. So that leaves Darwinism with no leading apologist. So now what?

  326. Lizzie:

    I’ll assume you’ll look at my response at 47.2.1.1.7 above.

  327. Lizzie:

    I’ll assume you’ll look at my response at 47.2.1.1.7 (Sorry, I got it in the wrong spot the first time around)

  328. gpuccio:

    I think what is obvious to you, is not obvious to EL and DrBOT.

    When it comes to neutral drift, you have clearly, and correctly, said that this amounts to no more than a “random walk”. And the implication, then, is clearly that: “In that case, the system is acting randomly, there is no selection, no amplification,” which, of course, means that almost nothing can happen given the known improbabilities for dFSCI. They’re missing this point entirely.

    Instead of blind faith in NS+RV, it’s blind faith in RV. Once faith is blind, what’s the difference?

  329. gpuccio:

    We here in the US say that “it’s like banging your head against the wall” when referring to a situation where the person your speaking with just doesn’t want to, or just doesn’t understand, what you’re trying to tell them.

    I think you’ve “bang[ed] your head against the wall” for the nth time. You better stop. Advil only helps so much! ;)

    I must say, that, having run out of patience long ago, I’ve decided to “bang [their] head[s] against the wall”. It’s a lot more fun that way. :)

  330. PaV:

    Thank you for the psychological support :)

    It’s beautiful to know that at least someone cares about my poor head…

  331. Petrushka:

    That is just a hidden version of why are there no intermediates among contemporary organisms. Why should there be?

    A simple question, a simple answer.

    Let’s say that a transition from one basic domain to another, at some point of natural history, “helped” by NS, is of the form:

    A – A1 – A2 – B00 – B0 – B

    With “A1 – A2 – B00 – B0″ all being naturally selectable intermediates, each of them giving a reproductive advantage, xand therefore selected, expanded and fixed.

    In the modern proteome, we have A. We have B.

    But we have no trace of A1 – A2 – B00 – B0. Not in some particular case, but in the general case. I would say without exception.

    Why?

    Now, don’t come and say that what we are observing are the modern proteins, and similar nonsense. I have shown you, with examples, how those “modern proteins” show amazing homologies even between the bacterial and the human form (that I would take as the two extremes of observable evolution). I hope you may agree that the only meaning of that is that they still have amazing homology to their very old precursor in LUCA, more than 3 billion years ago.

    So, we can see in the proteome the very clear traces of what existed in the old times. We do see them all the time.

    If, for a whole supposedly rcih category of molecules (the “bridging intermediates”) we can find no trace in the proteome, what is the only reasonable explanation?

    I supppose a three year old baby is already answering: they never existed.

  332. I had already addressed those points in my post #50 (to you).

    well, not really, otherwise we wouldn’t be where we are

    .. neutral mutations in no way change the probabilities of a random walk, and neither does genetic drift, because it is a purely random event, and therefore does not change anything.

    That just reads as incoherent to me – but I’m starting to see the problem …

    IOWs, if we must consider the pobabilities of a random walk from A to B (unrelated), all the states have similar probabilities of being reached, both with or without drift.
    That’s why I always say that drift is irrelevant to the computation of probabilities, and favours no specific configuration, least of all a functional one.

    You appear to be treating drift as a type of search …

    any time you reach an unrelated state through a random walk, by neutral mutations, drift, frameshift mutation, inversion, translocation, ot whatever, the probabilities that such a state is functional are 1:10^140.

    Why are you talking about random walks and neutral mutations? Neutral drift is not a random walk. A random walk will take you in any direction and can result in a change if reproductive potential (selection can act). A neutral mutation is just those steps that do not result in a change of fitness.

    Neutrality is a feature of the evolutionary search space – it is defined in the context of fitness, of which heritable elements are subject to selection, so it cannot be treated as something different, it cannot be ignored in your calculations.

    a) the search is not local. It is a random walk that has to necessarily traverse the space

    Ok, you got several things wrong here. First, neutral drift is not a random walk, it is not the exploration of the whole search space, it is just a local move within the search space that does not affect fitness.

    Second, and only incidentally, a random walk is, by definition, a local search because it proceeds by moving in small steps across the search space – with each iteration there can only be movement in the immediate locality. By comparison a random search is one where the search space is sampled at random – with each iteration there can be movement to any other location in search space. Both of these can navigate the whole search space, its just that the random walk can only search the local space from one iteration to the next.

    Not good, eh?

    No. I think the best way to explain where you are going wrong is with a direct, if simplistic, example designed to illustrate how neutrality influences evolutionary search dynamics.

    We have a ‘genome’ (deliberately in scare quotes) that consists of two finite integer values – so our search space is two dimensional – and we have a fitness value at each location (fixed, rather than dynamic for the sake of simplicity)

    The grid of values below explicitly defines the fitness landscape (the x axis is one ‘gene’ and the Y axis is the other) and the value in each cell is the fitness at that (x,y) point. With each step (generation) a mutation can occur on only one axis (gene) and to a magnitude of +/- 1.0 in other words, in each step a mutation can only move us in ONE of these four directions: North, South, East or West.

    Here is the fitness landscape (hopefully formatted correctly because this ASCII art works best with a fixed width font! )
    Directions:
    N
    E W
    S

    Landscape:
    00000000000
    01111111110
    01222222210
    01233333210
    01234443210
    01234543210
    00123432100
    00123432100
    00123432100
    00123432100
    0012×432100
    00012321000
    00001210000
    00000100000
    00000000000

    For the sake of argument, lets start at the position marked with an x (where you have a fitness of 3).

    From here there are four possible directions a mutation can take you: N, S, E, W.

    So, for sake of argument again, a mutation takes you E -> you now have a fitness of 4 (consequently selected for by NS because you are fitter – you have climbed up the fitness hill)

    Now, again, you have four possible directions that mutation can take you. N results in fitness of 4, all other directions will result in a fitness of 3.

    N therefore is neutral (no change in fitness) but all other mutations are deleterious – NS selects against mutations that are deleterious – ones that take you S,E or W.

    From here there is no way up, no way to increase fitness through a single mutation, BUT any mutation that takes you North is not selected against because it does not reduce your fitness. The ONLY way you can move is North WITHOUT reducing fitness and consequently subjecting yourself to the filtering effect of NS. ANY mutation except a northward one is deleterious and selection will act – your reproductive success is reduced by these mutations. Drift is any movement north – any movement that does not invoke selection, that does not affect your reproductive success.

    In this situation you are on a fitness ridge – a flat path across the landscape with lower fitness areas on each side. Any move off this ridge will be punished by NS so the effect of mutations over time will be that you drift forwards and backwards along this ridge because natural selection acts to keep you in this neutral zone. If you drift far enough north you end up on the side of a fitness peak and then a further northward mutation will actually increase your fitness.

    Now compare the previous fitness landscape to this one:

    00000000000
    01111111110
    01222222210
    01233333210
    01234443210
    01234543210
    00123432100
    00123332100
    00001210000
    00123332100
    0012×432100
    00012321000
    00001210000
    00000100000
    00000000000

    The landscape is identical except that the neutral ridge is missing.

    So, start again – you start at X and mutate East – to a fitness peak of 4 – now a mutation in any direction will reduce your fitness, and be selected against.

    Now do the math: What is the probability of reaching a fitness of 5, from the starting point x, within this landscape compared to the previous landscape, using an evolutionary search?

    One important thing to take note of is that both landscapes have neutrality – for example a mutation that takes you around the side of a fitness hill rather than up or down is neutral. The difference is the ridge, these types of search space features are sometimes referred to as neutral networks – networks of neutral ridges connecting areas of the search space. They are a feature of the search space and represent degrees of freedom with respect to selection.

    It is a relatively easy task to turn the the examples above into a simple computational model and do some tests. If you explicitly define some different landscapes, with and without neutrality, seed a population to low fitness areas and apply a super simple GA, you can see the effect of neutrality on the evolutionary process. This should make it perfectly clear why the degree of neutrality, and the existence of neutral networks within a fitness landscape has an important effect on the evolutionary process.

    It’s nonsense. It’s wrong. Try to motivate it, or remain silent. Anyway, I will not explain the same things for the nth time.

    Nor will I. The example above should be more than enough for you to understand where you are going wrong – I would encourage you to work through the two examples, they are similar to, and pitched at the same level as, introductory lectures for year 1 CS students studying evolutionary algorithms.

    If you calculate probabilities about neutrality as if it is a random walk across the entire search space then you are not calculating the probabilities of evolutionary mechanisms finding a solution, or the effect of neutral networks on the search. This is what Elizabeth what trying to explain when she pointed out that you cannot carve neutrality off from selection – because it is defined by selection, and it is not a random walk.

    In order to calculate the probabilities you actually need to know how much neutrality there is in the landscape – how many sequences link one protein to another via a series of single steps that do not significantly affect fitness.

    IF a near neutral ridge like this exists then natural selection can act to ‘walk’ the sequence along this ridge.

  333. I must say, that, having run out of patience long ago, I’ve decided to “bang [their] head[s] against the wall”. It’s a lot more fun that way. :)

    I can’t say I agree that subjecting people who’s arguments you disagree with, or don’t understand, to physical violence is ever justified – and I certainly don’t view violence as ‘fun’ like you do.

  334. We known that language evolves, because we have written records documenting the emergence of languages like English. and yet we have languages like Basque, for which there is not know precursor. Is that evidence of a miracle, or intervention?

    It is always possible for cousin lines to become extinct.

  335. Basically you have lines where the cousins have gone extinct and lines where they haven’t. Cousin extinction is speciation. What you refer to as the origin of protein domains is an example of speciation.

    That’s why your argument is a gaps argument.

  336. For dFSCI computation, you need a purely random system

    So when you are wrong about something, you simply make up something, like protein domains being poofed into existence.

    150 bits. Poof. Rather than look to known and observed phenomena like cousin extinction, you assert that you know the true history of isolated lineages.

  337. DrBot:

    First of all, thank you for your detailed answer. This is exactly the kind of explicit and detailed response I am looking for, and I appreciate it. I allows discussion to grow.

    I will try to address your points.

    You say:

    You appear to be treating drift as a type of search

    No. What I said is:

    “if we must consider the probabilities of a random walk from A to B (unrelated), all the states have similar probabilities of being reached, both with or without drift.”

    I am not “treating drift as a type of search”. I am only saying that in a random walk of the kind I have proposed as a model (from an existing basic protein domain A to a new, unrelated protein domain B) the probabilities of reaching B remain the same, either drift is part of the scenario or not.

    Please, note that genetic drift is not the same as the existence of neutral mutations, as you seem to argue in your examples. Drift is a very specific kind of random amplification of some neutral trit, in sexual reproduction.

    From Wikipedia:

    “Genetic drift or allelic drift is the change in the frequency of a gene variant (allele) in a population due to random sampling”

    In all your post, you give no discussion of genetic drift, only of simple neutral variation.

    But that is not important. My point, that I maintain fully, is that neither neutral variation not genetic drift in its proper sense change the probabilities of a random walk in the model we are discussing.

    Let’s go on.

    Why are you talking about random walks and neutral mutations? Neutral drift is not a random walk. A random walk will take you in any direction and can result in a change if reproductive potential (selection can act). A neutral mutation is just those steps that do not result in a change of fitness.

    I am talking about random wlaks because that’s exactly what a transition as I have described is. Unless NS acts.

    I will be more clear. What we are discussing is the emergence of B (a new unrelated basic protein domain, with a new function and structure) from A (an existing functional protein domain).

    OK?

    Well, as the “engine” of the transition is RV (in all its forms), and as the searach space has to be traversed by definition (the two states are unrelated, and therefore distant in the search space), it is a random walk.

    Each variation event is random. They may have different probabilities (IOWs, the probability distribution of the events need not be uniform), but the events are random all the same.

    Another aspect of the problem, hoever, is what happens after a variation event. As we are talking of a reproducing population in an environment, NS can and does act.

    So, while with regard to pure RV the random walk is a purely random system, as soon as we take into account NS the system becomes “modulated” by the effect of NS.

    But what are those effects, and when does NS act?

    Here, we have to make distinctions, and be analytic. Recurring to poetic phrases like “differential reproduction of inherited traits”. We must ubderstand well how things work.

    So, the variation event can be characterized according to two parameters:

    a) is it local or not?

    b) what are its effects on reproductive potential?

    About a) you seem to assume that all variation events are local. That is not really true. Some forms of variation are not local, as I have already pointed out. A single framshift event, for example, is not local, and determines a sudden random “jump” in the search space. But,as my point is that both local and non local events have in the end similar probabilities of reaching B, I will stick in the discussion to local events, like SN mutations.

    About b), you will agree that they can be classified in three sets:

    a) Those that have no effect on reproduction

    b) Those that have a detectable negative effect

    c) Those that have a detectable positive effect

    Let’s make another assumption: that protein A is importnat for successful reproduction, and therefore significant loss of its funtion will result in b).

    Now, is NS acting?

    In the beginning, the only function available is the function of A.

    The main effect of NS on an existing functional protein, well documented, is to act as negative selection: the variations that strongly affect function will be eliminated because of reduced, or absent, reproduction.

    The main effect of that is that a protein can change to a point its sequence while retaining its structure and function. That’s why the same protein is usually more different in distant species, while its function remains the same. Let’s call that process “traversing the functional island”.

    It is possible that local variations give an increase of the function of A, but that is much more difficult, and anyway it could bring only to the “tweaking” of the existing function, or at most to the emergence of a new function with a different active site in the same family. For the moment, we will not discuss that, because it is not relevant to the discussion of how to reach B. Unless you can show that a more functional A is a step towards the sequence of B.

    Because, you see, we are talking very specific objects here: proteins, with specific biochemical roles integrated in the general scenario. And we must always be consistent with this premises.

    So, the detectable effect of neutral variation plus negative selection on an existing functional protein will be the “traversing of the fucntional island” in the course of naturla hisotry. the function remain the same, the sequence changes to a point.

    Is that a random wlak towards B? Absolutely not. B will be never reached that way.

    Because, to reach B, we have to traverse the genral search space, that is we have to go beyond the local sequence space, and dive in the sea of unrelated states.

    The way darwinists usually try to solve the problem is through the model of “duplication”. A is duplicated and becomes non translated, or however non functional. The original A maiontains the existing functionality. So, the new A, let’s call it A’, can change without the limitations imposed by negative NS.

    OK?

    Now, that makes practically any variation of A’ “neutral”, except for those variation that implement some new useful function, luckily associated with persisting translation.

    IOWs, any variation is neutral, until we reach B. Or B00, or B0 (some functional, selectable precursor of B). At that point, the remaining problem would be the transition form B00 to B.

    But now it is perfectly true that the search space can be freely traversed by NS, because there is no more the limit of negative selection, defending the functional island of A. It is true, as you say, that the initial variation will remain local, but as neutral variation accumulates, we are diving into the sea of unrelated states.

    And we can, now, reach B. But the probabilities are exactly those deriving from the total dFSCI of B. Or of the functional internediate, if and when it exists.

    So, you see, you model of GA has really nothing to do with the real biological scenario. The reason is simple: it is a bad model. In no way it has the form of what it pretends to model. I could comment on it further, but why? It is completely non relevant.

    I will stop here, for the moment. There are many other things that should be said, but I am interested in your comments about these first ideas.

  338. Thanks for the response, I’ll try and respond myself but it may be a day or two before I can – I have family duties to attend to this weekend :)

  339. DrBot:

    Please take your time :)

    I only hope to see your answer in the sea of unrelated posts this blog has become… In case, give me some (intelligent :) ) signal!

  340. I’d better chip in here, as I have, in fact, desribed drift as a random walk :)

    But this is where we have to be so careful of these metaphors. The sense in which “drift” is a “random” walk is when it is the description of the changing prevalence, over time of a specific genotypic variant.

    However, the “drift” of a phenotype across a fitness landscape is not, as Dr Bot says, a random walk.

    I do think in these discussions it is very important to be clear when we are talking about genotypic variants (which, in a sexually reproducing population, can propagate through the population independently of other variants) and when we are talking about the fitness of a phenotype.

    So Dr Bot’s example a “fitness landscape” defined as a two dimensional landscape along two genes. Let’s call that “gene space”. What he is showing is movement within that “gene space” by a phenotype, or, more strictly, by a population of phenotypes, the most prevalent pair of alleles within that population at any given time being given by the coordinates of X.

    Clearly, the traverse of the phenotype population across that “gene space” is not a “random walk” but is highly constrained by the topography of “gene space”, and will go along in preference to down, and up in preference to along.

    However, if instead we examine the traverse of each allele (i.e. each gene “state” as defined as a point on the axes of “gene space”) through “population space”, defined with generations on one axis and prevalence on the the other axis, we will observe a “random walk”, where the prevalence of that allele in the next generation may be equiprobable (if the allele confers no increase or decrease in probability of reproductive success relative to other alleles), biased in favor of greater prevalence (if it confers an increased probability of reproductive success) or biased in favour of reduced prevalence (if it confers a reduced probability of reproductive success).

    As Dr Bot says, you cannot carve neutrality of from selection. “Selection” is the name we give to the aspects of differential reproductive success that tends to keep populations “high” (on a ridge, up a slope) (I prefer myself to think of the landscape the other way up, with “gravity” as the analog of “selection”, and populations tending to roll down slopes or along plateaux, but that’s maybe just me :)), whereas “drift” can be used either to describe the “movement” of a population along a ridge or across a plateau, or to describe the propagation of alleles through a population. It is only in that last sense that it can be described as a “random walk”,but usefully so, IMO, as it underlines the fact that what we call “selection” is a highly stochastic process, and one that is not simply a property of the allele (a simplifying assumption made in some population genetics model) but of the environment in which the phenotype has to survive, as well as the internal “environment” of the allele (other alleles with which it finds itself in combination in a given phenotype).

  341. PaV:

    Lizzie:

    I’ll assume you’ll look at my response at 47.2.1.1.7 above.

    Yes indeed :) It is not my intention to evade responding – I just need to spend more time at my own site, and try not to start more hares here!

    Lizzie:

    Sorry for taking so long to reply. I must admit that with this new format, and with the sheer number of posts taking place each day, it’s very hard to keep track of where I’ve left an entry. (Hope somebody’s taking note) But, I’v also been away from a computer for a couple of days.

    Yes, that’s one reason I would welcome people here dropping by at my own site, where things move a little more slowly! Not trying to poach, just trying to provide a more leisurely environment for longer conversations:

    http://theskepticalzone.com/wp/

    Would be delighted if you dropped by :) OK:

    I don’t know what you call it, PaV, and I don’t care very much; the important thing is that it’s a key part of modern evolutionary theory.

    Certainly neutral drift is part of “modern evolutionary theory”; however, it has serious problems—which you seem to deny for whatever reason. But let’s move on.

    Well, I’m not sure what those “serious problems” are. It is a fairly straightforward observation that the distribution of novel variants tends to peak near neutral, and that near-neutral variants have a sporting chance of replicating them selves in substantial numbers in the population, despite conferring little or no phenotypic advantage, and despite possibly being mildly deleterious, as I point out below:

    What we now know is that the vast majority of new variants are near-neutral, which means that any given population at any given time represents a pool of phenotypic variants of which some variants may prove more successful than others in surviving when the enviroment changes.

    This is probably true—given enough time for drift to work.

    You seem to be stuck in your agency metaphor! “Drift” doesen’t need “enough time” to “work” – it isn’t an agent, any more than “positive selection” and “negative selection” are agents. They are simply ways of describing differential reproductive success. If a genetic variant makes no difference to the phenotype’s chances of reproducing successfully, relative to that of its peers, we say that it is “neutral”; if does make a difference, we say that it is either “beneficial” or “deleterious”. But these are not discrete categories, and all “drift” through the population or out of it. However, a variant the tends to enhance the probability of reproductive success will have a “bias” to its drift – will be a little more likely to become more prevalent than a neutral variant would be, and vice versa for a variant that tends to lead to reduced reproductive success. In other words the whole notion of “Natural selection” really needs to be seen as a stochastic “drift” process, in which some variants, in some environments, have greater or lesser chances of becoming more prevalent than others.

    But, is the mere ‘presence’ of such ‘successful variants’ sufficient. Obviously the ‘presence’ of these putative ‘successful variants’ is necessary. But is it also sufficient for macroevolution to take place? We continue . . . .

    This means that when we set up Darwinian computer models, we find, to our surprise, that complex functions evolve more readily than perhaps Darwin might have anticipated because necessary but neutral precursor variants are already likely to be there in the population.

    Is this true? Do ‘Darwinian computer models’ actually show this? Behe and Snoke set up what they considered to be a ‘Darwinian computer model’ and they got no such result—in fact, it showed even NS, let alone neutral drift, was rather impotent to bring about meaningful changes.

    Well, it won’t always happen, clearly. The issue is whether it can happen. And Lenski et al, with AVIDA, showed that it can – i.e. that useful functions (useful to the organism) can evolve even if necessary intermediate steps are neutral or even deleterious. If there are no beneficial intermediate steps, then the function is clearly extremely unlikely to evolve, and Darwinian processes will work no better than a random draw.

    So the issue is not whether Darwinian process can work (we know they can) but whether they will work on the kind of fitness landscape that biological organisms inhabit. What AVIDA shows is that those fitness landscapes include landscapes with substantial plateaux and horizontal ridges, and even some ravines, not just landscapes in which all peaks are reachable by steady climb.

    But let’s say that what you say is true. Well, what you’re saying is that the “necessary” neutral precursor (variant) is already likely there. Okay. But, as I said above, the variants are necessary, but are they sufficient to explain evolutionary change?

    This is where the whole idea of “fixation” comes in. You’re simply assuming that because this ‘beneficial’ (I know, ‘beneficial’ relative to the ‘current’ environment) is there, the rest automatically takes care of itself. But this is where, IMHO, you’re going wrong. The next step—which is ‘necessary’ and ‘sufficient’—is for this ‘beneficial variant’ to become fixed, wherein, every member of the population shares this variant.

    No, “fixation” is not necessary. Indeed, the fixation of a neutral allele (and certainly of a deleterious one) is a problem for a population and thus for small populations where fixation is more likely. Fixation means that potentially useful variance has been lost. What makes it more likely that a useful function will evolve via neutral steps is simply that there are plenty of instances of those neutral steps, because the more opportunities there are for the next beneficial step to occur, the more likely it is to occur.

    This is because, let’s say, a little kitten, born with a ‘variant’ that allows it to sniff out potential prey better than any of the other cats around, has a likely reproductive advantage over its litter mates as an adult. And so, too, would its offspring. But what if, one day, while still a kitten, it became distracted while crossing the street, and was run over. What, then, of this ‘beneficial variant’? What becomes of it? ANS: Nothing. It’s lost to the population.

    Sure. That’s what I mean by “selection” being a highly stochastic process. Many novel potentially beneficial variants may well be lost before their bearers even have a chance to reproduce. This is why it seems much more likely to me that most advantageous variants probably start as neutral variants, and become advantageous long after they have a history of substantial prevalence in the population. In other words that most “beneficial variants” are not novel at the time they become beneficial. I realise that this may be a someone unusual way of looking at Darwinian evolution, but it seems to me to make sense of what we know. More importantly, we observe it in the field (and lab) as what you call “microevolution” – the increased prevalence of already existing variants in response to environmental challenge. My point is that this feed of potentially useful (but currently neutral) variance is being constantly drip fed into the population and propagated by drift, so that “macroevolution” is simply the same process as “microevolution” but with a sustained movement in a single direction, rather than oscillation around a mean, and driven by sustained, rather than oscillating, environmental change.

    This is a random event, and this randomness—that is, the potential for a single member of the population to be accidently lost, or, for whatever reason, not be able to furnish offspring; or for the offspring themselves to be killed off or reduced in number—all these random kind of events need to be overcome by the population. And that’s why population geneticists calculate such things as “fixation” times. Once a variant is incorporated into the entire population, it’s very likely not to be lost very easily. And now the population, as a whole, can work on acquiring—and fixing!—the next variant. But how long does this take?

    Well, Kimura did the calculations, and it turns out to be 1/4N_eff. And, hence, in 49.1 below, I include a sample calculation from Kimura’s magnus opus, “The Neutral Theory of Molecular Evolution”. It turns out that this is a very slow process.

    So……the mere appearance of a ‘beneficial variant’, though ‘necessary’, is not sufficient. Fixation is also a necessary, and somewhat sufficient condition for macroevolution to occur. The problem though is that this “fixation” process works way too slowly to account for the fossil record. This is only more so the problem when considering chimp—human differences (only 4 million years for all these “fixations” to occur!)

    Well your error, IMO, is assuming that “fixation” is a necessary condition for selection. It isn’t. Clearly, the more examplars of a novel sequence exist in a population (the more organisms that carry it) the more likely it is to hang around. This is what Kimura’s equation tells us. So the earliest generations of a novel sequence are the most risky – the more established it becomes, the less likely it is to be lost, just as the more people are told a secret , the more difficult it is to suppress it.

    And the more examplars there are of a novel but neutral sequence, the more likely it is that a subsequent mutation that renders it beneficial is to happen simply because even rare events come close to inevitable given enough trials.

    But what it does mean is that the old cliche that mutations are random and natural selection isn’t, is pretty well meaningless (and I wish people, especially Dawkins, would stop saying it!)

    Dawkins is the leading apologist for the Darwinian cause. His entire argument falls apart if NS is considered to be ‘random’. Per your view, his arguments fall apart. So that leaves Darwinism with no leading apologist. So now what?

    There are plenty of “apologist[s] for the Darwinian cause” but more to the point, it doesn’t “need” apologists, it “needs” good scientists, which it has, aplenty, by which I mean there are plenty of evolutionary biologists in the world all doing sound work, refining and modifying evolutionary theory. However, Dawkins’ argument doesn’t “fall apart” of NS is considered “random”. As I keep saying, “random” is a non-specific word that needs careful definition if it is to be used in a technical sense. I think Dawkins misuses it, in an attempt at simplification, and, in so doing, sets up a straw man.

    NS is not “random” in the sense that it refers to a process in which the survival of a given phenotype is not equiprobable for all genotypes. That’s why it is called “selection”. However, that doesn’t mean that selection is not a stochastic process, as your kitten example shows.

    And “RM” is only “random” in the sense that novel variants are not more likely to be generated simply because they would be useful in the current environment. In that sense, novelty generation is “blind” to current needs. However, that does not mean all possible novel sequences are equiprobable (and this means even if we use the word “random” in the sense of “equiprobable” in relation to NS, it does not apply to RM). Novel sequences very similar to those of the parent sequences are much more probable than very different sequences, and as the parents are, by definition, fertile, the probability of producing fertile offspring is much more likely than the probability of producing non-fertile offspring.

    But far from “fall[ing] apart”, correcting Dawkins’ simplification means that the Darwinian proposal makes more sense, not less, and maps on to what we actually observe – novel variants that are strongly biased in favour of near-neutral phenotypic effects, and beneficial variants being pre-existing neutral variants now proving benefical in a novel environment, or possibly in a novel genoetype.

    I’ll keep checking in here for replies to my posts, so if you have a reply, I’ll gladly respond:)

  342. I’m chastened. And amused.

  343. Just another note: drift does not “enrich” anything. If a neutral mutation es expanded by drift, other neutral mutations are lost in that expansion. There is no enrichment.

    By “enrich” I simply meant that neutral mutations are constantly present in substantial numbers in the population, representing potentially useful variance. Yes, some will be lost as others are gained, but that means there is homeostasis as regards variance, and the larger the population, the larger the variance.

    Drift is absolutely useless, or at least it does nothing different from what other kinds of RV do: it randomly changes the existing sequences.

    We seem to be talking about radically different things. I am not talking about anything that “changes the existing sequences”. I am simply talking about the propagation of novel genetic variants through a population.

    We cannot even say that drifts accelerates the rate of variation. First of all it is a rare event. Other forms of variation are much more common.

    I’m at a loss, gpuccio. Could you say how you are defining “drift”? What is a “rare event”? It happens in every generation of a population! In other words, in every generation, neutral alleles will change in prevalence. Some will drop out completely. Others will be represented for the first time. But that drift process never stops. How could it?

    Secondly, we know well that too much variation is worse than too little. That is well known, I believe, in population genetics. You cannot increase your chances of reaching new functional targets only by increasing the rate of variation, be it by drift, or by any other means.

    You seem to be talking about mutation rate, not drift. Sure, there is probably an optimal mutation rate. But isn’t what we are talking about.

    Just an example of how drift can be in the same way useful or deleterious, so that its global effect is nil.

    I’m really not following you. Do you mean mutation or what? I’m not sure what the antecedent of “its” is in the above sentence. “Drift” is used to describe the change in prevalance of alleles from generation to generation when the alleles are near-neutral. But because neutral variants can so “drift”, and because neutral mutations are very common, it means that there will always be plenty of potentially useful variance in a population should the environment change.

    Let’s say that to reach B you need serine at position 126. Well, you get lucky enough and get that mutation in A. It is not amlified, but luckily it is neutral, so it is not lost too. It is there, ready to contribute to the final result (provided that other lucky events accumulate).

    Now, if by further luch that neutral mutation is expanded by drift, we will certainly be nearer to the goal.

    Well, yes, if that mutation occurs it may well increase in prevalence purely by drift, increasing the probability that the next “lucky” event will occur in at least one bearer.

    But in the population there are many other neutral mutations. After all, as you say, neutral mutations don’t tend to favour what works better.

    Sure. But that doesn’t matter. What matters is that there are a substantial number of instances of the A mutation in the population, because the more there are, the more opportunities there are for the a beneficial mutation to occur in one of them.

    Now, let’s say that for once you are not lucky, and the neutral mutation that is expanded by drift is one, in another individual, that has glycine at position 126.

    I am really not following you. Lots of neutral mutations can become more prevalent by drift. Or are you talking about asexually reproducting populations?

    Now, that is a neutral mutation for A, but it is not neutral at all for the future target, B. Indeed, let’s say that with glycine at 126, B will never be functional.

    Now, if the neutral glycine is expanded by drift, instead of the neutral serine (they have the same probability, after all), what has happened? You have lost the favourable neutral mutation that had already accumulated.

    That is the truth for neutral mutations and genetic drift. They don’t change the explanatory scenario.

    The only place where they are “useful” are the wrong arguments of darwinists.

    tbh, what you are saying seems to me extremely muddled. I’m not sure if it’s a jargon problem, or what, but I can’t even parse what you are saying.

    Are you talking about sexually reproducting populations? And by “amplified” do you mean, is reproduced in lots of individuals? Or something else?

    Let me give a toy example, assuming a sexually reproducing population of 5000:

    Let’s say that if mutation B occurs in the same individual as mutation A, the effect is beneficial for the phenotype, but that neither A nor B alone confer any reproductive benefit, nor disadvantage

    Let’s say A occurs, and happens to an individual who happens to produce several viable offspring, all of which go on to have further offspring, resulting, over a few generations, of 1000 individuals bearing A. Now B occurs in an individual without A. This individual also reproduces successfully. Eventually, one if its B bearing descendents mates with an A bearer, producing offspring with A and B. These then produce lots of offspring, increasing the number of A and B alleles in the population. Whenever they occur in the same individual, that individual has lots of extra offspring, and eventually both A and B become “fixed” and every member of the population has both, benefiting from the resulting phenotype.

    Now let’s take a cloning population. Here, B has to occur de novo in an individual that already has A. But the more A individuals that exist the more chance there is for B to occur in at least one of them. So again, providing A doesn’t do any harm, there’s a good chance that there will eventually be lots of individuals with A, each additional individual increasing the probability that one of them will end up with B mutation.

    So either way, the fact that neutral mutations can drift increases the number of opportunities for a second mutation that converts the first into a benefit to occur. No?

  344. DrBot:

    May I please respond? Let me get to the point. The model you propose looks nothing like what evolution in the real world looks like.

    While this example is apparently used to instruct students in the use of evolutionary algorithms, sadly, what is being programmed is an unrecognizable facsimile of what actually takes place. It amounts to a semi-sophisticated, computer-generated, “just-so” story.

    I will only make two observations here to make my point:
    (1) your putative “fitness landscape” looks nothing like the real world—-real-world, actual, fitness landscapes are extremely steep. I recently looked at a paper that couldn’t have been more than two years old. In it was a graph that was comparing fitness levels to some other parameter. It was basically a fitness landscape along the horizontal portion. For, IIRC, this protein, or perhaps a protein cluster, the fitness landscape was a straight-up vertical line! Stuart Kaufman gave up on the idea of these kinds of landscapes because they were too steep to climb. So, your example—with 3s, 4s, and 5s—has nothing to do with biological reality, I’m afraid
    (2) While saying that moving from 4 to 3 is a deleterious mutation, you’re basically covering up, again, perhaps unintentionally, the fact that we’re really not talking about a fitness level that goes from 4 to 3, but from 4 to (-4). This is consistent with the point I’ve made in (1) above. That is, in the portions of any protein domain that codes for functionality, one amino acid substitution is sufficient for near loss of function, or even complete loss of function. You can easily go from 100% function to .001% of function. This isn’t 4 to 3.

    Because of (1) and (2), you need to have very specific amino acid substitutions that produce beneficial effects. This obviously has to occur in the functional portion of the protein domain. But this is exactly the portion of the protein sequence that is the “steepest”, and the most likely portion of protein sequence where negative selection will occur. The effect of all of this will be that any “beneficial” mutation in an individual—assuming that several amino acid substitutions must occur for a new protein function to arise—can be easily overcome by a “deleterious” mutation before the next “beneficial” mutation arises, and, thus, the whole leading to the loss of that lineage. This is partly why it takes 1/4N generations for a neutral mutation to become fixed.

    Now, if the population is small, then getting the “neutral” mutation at just the right place will take a long time. OTOH, if the population is large, then it takes a long time to “fix”. And, if it’s six, or seven, amino acid substitutions that are needed to move from one protein domain to another, this represents a long period of time. I’ve done some calculations in the past, and I think the optimum population size is around 500,000; which is just the population size Kimura used in the example I cited above. So, for six needed, mutations, based on a yearly reproductive cycle (Kimura’s numbers reflect a two-year reproductive cycle), this amounts to 6 x 3.5 million yrs. = 21 million years for a single protein to develop a new function via neutral drift (negative selection is presupposed in all of this).

    So, by not including either the number of mutations that will be required, or the problem of fixation*, or the amount of time either the generation or fixation of the mutation will take, you’re not anywhere near simulating a real biological example of evolution.

    Isn’t this really the problem with most EAs? Of, if it reasonably simulates actual real-world evolutionary conditions, then the amount of real information/function it produces is negligible (and always subject to other assumptions which can sort of sneak function/information in.)

    ______________________________________________________

    * The “problem of fixation” is this: unless the new a.a. substitution is “fixed” in the population, then the individual in whom the first a.a. substitution took place—we’re here assuming this is taking place via neutral drift—has no selective advantage, and so there’s no certainty whatsoever that this potentially helpful neutral mutation (PHNM)will spread. So, there will be only a small number of individuals in the population having this PHNM. Now what is the likelihood that the next PHNM will take place in these same, few individuals?

    Some numbers: N = 100,000; n = number of individuals with the first PHNM = PHNM1 = 100 = 0.1% of the population; genome length = 10^9 bp; mutation rate = 10^-7/generation; yearly reproductive cycle.

    Then, for PHNM2 to arise, we have: 100 x 10^-7 mutations/ generation/10^9 bp = 10^4 bp substitutions per generation. We need to cover the entire genome to be sure the PHNM2 arises. So, 10^5 generations will be needed = 100,000 years. However, in this period of 100,000 years, among these 100 individuals, 10^9 mutations will have arisen, of which, only one is the one we’re looking for. What is the likelihood, then, that these 100 individuals would have survived this period given that, on average, every location on the genome has had a substitution? Given that negative selection is always at hand, not very likely. If, however, the substitution is fixed, then the PHNM2 will arise much faster, and with much fewer deleterious mutations to contend with. But now we’re back to 3.5 million yrs. And so it goes.

  345. PaV, would you take a look at my comment above? I think there is a mismatch between what Dr Bot is talking about and what you are talking about.

    In DrBot’s toy example, the fitness landscape is in gene space and what “moves” in gene space is the phenotype. It is the phenotype that changes in fitness as it moves through gene space, not the gene, which simply exists in various states (represented by the two axes), which we call alleles.

    So, along the horizontal and vertical axes, each row/column represents a different allele which may give rise to a slightly different protein, or even a slightly more or less efficiently produced protein (there’s some evidence that even “silent” mutations have phenotypic effects).

    So when you say:

    (1) your putative “fitness landscape” looks nothing like the real world—-real-world, actual, fitness landscapes are extremely steep. I recently looked at a paper that couldn’t have been more than two years old. In it was a graph that was comparing fitness levels to some other parameter. It was basically a fitness landscape along the horizontal portion. For, IIRC, this protein, or perhaps a protein cluster, the fitness landscape was a straight-up vertical line! Stuart Kaufman gave up on the idea of these kinds of landscapes because they were too steep to climb. So, your example—with 3s, 4s, and 5s—has nothing to do with biological reality, I’m afraid

    You are only looking at a single slice through DrBot’s gene space.
    So to take your example – if, along a single dimension represented by alleles of a single gene, a neighbouring allele confers a large increase in fitness on the phenotype, then the population will tend to “move” to the top of that “cliff” (because individuals bearing that allele will out-replicate their peers, by definition). However, if, along that single dimension there is a local maximum, then it will be harder for the population to move from that local peak.

    Until we consider other dimensions (two, in DrBot’s toy example). For example, let’s take this one:

    22411
    14412
    14321
    14421
    13521

    And let’s say the phenotype starts at row 1, column 1, at fitness level 2. It does not move down the column, because that would mean going to a lower fitness level, and selection keeps it on its ridge. So it can drift to row 1 column 2 (a neighbouring allele of the horizontal gene) then leap up to row 1 column 3 (another neighbouring allele of the horizontal gene). Now, if we consider only that gene, it is stuck. There is a 5 on the fitness landscape, but it’s on the bottom row. However, if we consider the vertical gene, there is a route to the 5 that does not involve going down hill. It’s not a straight route, but it exists. And the more dimensions you add (and there will be one for every gene, and that’s before we consider new genes, and of course each dimension will be much longer than five alleles) the richer the network of ridges between peaks. That is DrBot’s point – that high dimensioned (even two dimensional) fitness space offers orders of magnitude more possibility from getting from one peak to another.

    As for some “slopes” being “too steep to climb” :) The kind of fitness landscape that is difficult for evolutionary processes to traverse are not landscapes with steep slopes, but landscapes in which there are too many plateaux and canyons between the bases of the slopes. Once you are at the base of a slope, it doesn’t matter how steep it is. The issue is how you get to the base of the slope (or the edge of the cliff if you turn it upside down).

    (2) While saying that moving from 4 to 3 is a deleterious mutation, you’re basically covering up, again, perhaps unintentionally, the fact that we’re really not talking about a fitness level that goes from 4 to 3, but from 4 to (-4). This is consistent with the point I’ve made in (1) above. That is, in the portions of any protein domain that codes for functionality, one amino acid substitution is sufficient for near loss of function, or even complete loss of function. You can easily go from 100% function to .001% of function. This isn’t 4 to 3.

    Well again, you seem to be confusing phenotype with genotype. Fitness is a property of the phenotype, not the genotype. Now it may be that some proteins are absolutely necessary for viability, and any mutation to the coding for them is disastrous. If that is the case, then clearly along dimensions orthogonal to that represented by that gene there will be a ridge. But that doesn’t mean the phenotype is stuck at a fitness maximum because there are other dimensions. It just means that that gene will be very highly conserved. Other genes are far more robust, which is why there are so many perfectly viable alleles in most populations, with near-neutral phenotypic effects.

    Conversely, it may be that some proteins are Irreducibly Complex, in which case they are sitting on a high butte in a flat landscape. But again, that doesn’t mean they can’t be climbed, because as DrBot points out, populations can drift along horizontal ridges, and if they drift to the base of a bluff, there is nothing to stop them ascending to the top.

    As for the “fixation” issue – sure, once an allele is fixed, it can’t drift out again. But that isn’t what matters. What matters is how many bearers of the allele there are. The more there are, the more opportunities there are for a subsequent mutation to occur that renders it beneficial.

    And the larger the population, the larger this number can be. It doesn’t matter if fixation is less likely, so is extinction, once the numbers are substantial, as Kimura’s equations show.

  346. Just briefly, whilst I have a few minutes to myself :)

    My toy example was not intended as a model of biology – and I didn’t present it as such. It is designed for the sole purpose of explaining how the topology of a fitness (or inversely, and error) landscape influences the probabilities of achieving certain states during a ‘search’. This concept applies to any search system and understanding in is IMO a vital part of understanding search systems in general.

    PaV – when you say it is not a good thing for comp-sci students to learn about because it is not an accurate model of biology you are missing two vital points. Firstly, it is a high level concept common to any search problem (including biology), and my example is designed to explain that concept in as simple a way as possible.

    Secondly – not all evolutionary algorithms are designed to model biology, they are widely used in engineering as tools for solving design problems, and again, understanding how fitness landscape topology affects search is vital if you want to deploy these types of algorithms effectively in real world settings – that is why many people study neutrality in fitness landscapes in detail, because it matters!

    I’ll try and post a more substantive response tomorrow afternoon – once I’ve done some of the things I am supposed to do in order to earn a living ;)

  347. PaV,

    Extremely interesting. I have long been sure that this would be the case, but I did not have concrete figures. I was looking for that sort of computations. Somewhere I read that somebody came up with this sort of estimates showing the practical impossibility of the evolution of the human eye. But I could not find the figures. Could you point to the paper(s) you talked about! Thanks.

    Maybe it’s mean of me but I am glad to hear Stuart Kauffman gave up on it :)

  348. Guys (Elizabeth, DrBot):

    First of all I want to thank you both for your intelligent contributions to this discussion. You are good interlocutors indeed.

    While we catch our breath, I would like to add a couple of comments.

    Much confusion in your answers is, IMO, created by the fact that you refer to models and context that are completely different from what I am discussing (the origin of protein domains).

    The differences are many, but I would like to list briefly the most important:

    a) A protein domain is a functional unit, and a complex functional unit. The mean length of a protein domain is more than 100 AAs, but many are quite longer. A protein domain has a very specific biochemical function. This function is what must be considered first when we discuss the origin of domains. A protein domain, being a functional unit, cannot be decomposed in simpler functional units. Most protein domains are certainly well beyond conventional limit of 150 bits for the dFSCI in biological systems.

    b) The infamous concept of “fitness function” is not good at all when speaking of protein domains. There is no simple or continuos fitness function that can be applied to that context.

    As we are discussing NS, the relationship between the specific biocemical function of a protein and the reproductive function can be very complex and indirect. That’s why, first of all, we must look at the biochemical function if the protein. That function must be present. It can be measured independently form the reproductive function. Therefore, we, as intelligent observers, can define and measure the biochemical function in precise and direct ways.

    But NS can “see” the single protein, both positively and negatively, only in the measure that the specific biochemical function of that protein is fundamental for reproductive fitness.

    So, indeed, a mutation can be negative, or positive, in the biochemical sense, and still be invisible to NS.

    c) Protein domains are isolated islands of functionality. They have different structures and different functions.

    Most of the experience in neutral evolution, so dear to Elizabeth, is derived form observation of the neutral evolution inside families. As I have already said in my previous post, that kind of evolution, although very important to assess relationships between species, doe not affect the function, or at most (but it can be debated, and is debated by Axe in his paper) could be repsonsible of small tweaks at the active site level, with changes of function but preservation of the general structure.

    That kind of model does not apply to the generation of new domains, where a whole and completely new sequence of more than 100 AAs arises.

    For that kind of event, only three models can be conceived:

    1) An existing, functional, transcirbed and translated gene gradually changes to a new gene. That is full of problems: fisrt of all the original function is rapidly lost, and it is not clear how NS would act, given the two different functions of A and B.

    2) The process happens in a duplicated, inactivated gene. In that case, it is not clear how NS can act at all, and the variation remains by definition neutral. All the probability barriers apply.

    3) The process happens in a segment of non coding DNA, possibly through transposon activity. All the probability barriers still apply, and NS cannot act (at least, not until a functional transcribed, translated protein does arise.

    My favourite model is definitely #3. That is the best model for design. And transposons are, at present, the best candidates for guided variation.

  349. We know from actual experiment that it is possible to select minimally functional sequences from a random library of sequences.

    Now which is the more rational assumption: quintillions of bacteria produce a minimally functional mutation every few million years, or that an invisible sky pixie drops in every few million years an poofs a sequence into existence.

    There’s no proof either way, but you can accept a process that has been observed, or one which hasn’t.

    I don’t believe you ever responded as to why you think speciation of protein coding sequences and the resulting isolation is a problem. I believe I asked about the Basque language and whether it was poofed into existence.

  350. Ok, I appear to have caught a bout of flu and now my brain feels like it is full of toxic mud, so rather than providing a long response I’ll just reply to a few key points for now – then have some pills and go to bed :(

    The first general point is that within a search space that is being traversed in small steps, in the way evolution does, rather than random bounds, in the way a random search does, the probabilities of getting from point A to point B scale with distance – this should be obvious really. The ‘search’ proceeds by taking relatively small steps in the local configuration space, resulting in some kind of fitness feedback (a change in reproductive success).

    Because of this within a given time period your probability of reaching a state diminishes with the distance of that state from your starting point.

    So, the probabilities depend on the relative co-ordinates of the two locations in configuration space.

    Second – because NS will act on ANY genome configuration that enhances or diminishes reproductive success, some locations in the search space are less likely to be traversed.

    If you think of in in terms of the islands metaphor:

    1 Above seal level is positive function (enhances reproductive success)
    2 At sea level is zero function (but not detrimental – just ‘does nothing’)
    3 Below sea level is detrimental (reduces reproductive success)
    4 Neutrality is ANY flat path or ridge (not necessarily the at sea level)
    5 And finally – go too deep (up to your neck) and you reach non viability (no reproduction at all)

    Basically NS prevents the search ever getting to a point more than waist deep in the sea – so the deep sea, the vast area of ‘dead’ genomes, never gets explored. Negative selection presents a barrier that locks out these parts of the search space and effectively makes the searchable space much smaller that the whole of the configuration space.

    This ratio of searchable space to search space is critical IMO. This is why you have to consider both the search space topology, and the nature of the search (i.e. localised/stepwise or random sampling) if you want to calculate meaningful probabilities.

    The distribution of probabilities for achieving any particular state from a given point and in a given time are highly dependant on how your search proceeds and the shape of the landscape you are traversing.

  351. I think it is a poor analogy to support the idea of biological evolution as the languages do not reproduce and because intelligent agency is directly involved in language formation. In any case it is no better than any artefact.

  352. Flu?

    Drink some emegence-c and some cell power- should be available at your local health-food store

    Three times a day- and if you continue this you won’t get the flu again….

  353. Eugene S:

    I suppose you’re talking about the fitness landscape being so vertical? If so, I regret not bookmarking it, and so I simply can’t remember where it was. It was in a paper that was considering something else; and I think that’s the only reason we see it in print.

    I, too, have long suspected–really, known–that this is what they must look like. But the EvBiol don’t want to look these things square in the eye. Yet, this is what fitness landscapes really look like.

    As to Stuart Kauffman: yes, he’s gone on to greener pastures. I suspect he might not come out and say that the rugged landscape approach has no merit; but the fact that he’s moved on says a lot.

    Should I come across the paper again, I’ll try to reference it here. It’s paper that’s come out within the last two years, IIRC. But that’s not narrowing it down too much, is it? I have to run . . .

  354. I have no time to do anything on this topic until this afternoon, which, per my location, is about 8 hours hence. Til then.

  355. Yes, I meant the vertical slopes of fitness. It would really be nice to trace that. Thanks anyway.

  356. gpuccio:

    My favourite model is definitely #3. That is the best model for design. And transposons are, at present, the best candidates for guided variation.

    This certainly applies to primates. And is probably the best suggestion of inherent design in the genome.

  357. DrBot:

    I respect your flu (I had one last week, and I am still not fine).

    So, brief comments:

    So, the probabilities depend on the relative co-ordinates of the two locations in configuration space.

    Exactly my point. The configuration space is the space of sequences. Do you agree with that? I ask, because that seems to be a very simple point that darwinists often forget. Variation acts on the sequence. More the sequence is different, more the proteins are far away.

    So, two sequences that have less than 10% identities are as far as possible in that space.

    Basic protein domains share less than 10% sequence.

    They are as far as possible in the space. The space has to be traversed, to go from one to the other.

    Basically NS prevents the search ever getting to a point more than waist deep in the sea – so the deep sea, the vast area of ‘dead’ genomes, never gets explored. Negative selection presents a barrier that locks out these parts of the search space and effectively makes the searchable space much smaller that the whole of the configuration space.

    Exactly my point. Negative selection is exactly responsible for keeping the search inside the functional island. That’s why existing proteins remain functional, and retain structure and function, thorughout natural history, even if their sequence changes because of neutral variation.

    That’s why we have so many different myoglobins, so many different aminoacyl tRNA transerases, that are essentially the same protein, although their sequences are sometimes different enough. That is calling “traversing the functional island”. Please, look at the followinf paper:

    “Sequence space and the ongoing expansion of the protein universe”

    http://www.nature.com/nature/j.....09105.html

    summarized here (the paper is not free):

    http://www.lucasbrouwers.nl/bl.....-universe/

    As the paper states, may proteins have not even traversed fully their own functional island.

    But again, that is what happens when A is functional and necessary: A, very simply, is preserved. Its sequence can change somewhat, but it is neutral change. IOWs, A does not go anywhere. It remains in its functional island.

    If that were all that happens, new proteins would never appear. Or at least, not new protein domains (As I have discussed, some microevolution, or let’s say “intermediate evolution”, implemented by changes of 1 – 8 AAs, could still happen, and we can discuss where really is the “edge” of unguided functional variation. Personally, I would stick to Behe’s 2 or 3 AAs).

    But that is not all that happens. New basic protein domains, as I have argued, have been appearing throughout natural history. Even in humans there are probably a few.

    So, where do they come from?

    Again, the “duplicated gene” and the “non coding DNA” scenarios seem the best. They both have three things in common:

    a) NS, both negative and positive, seems to have no role, or only a really minor role

    b) Neutral variation can easily happen, and can easily reach any possible target

    c) The whole dFSCI barrier applies.

    This ratio of searchable space to search space is critical IMO.

    Sure. That is the main point in dFSCI calculation. The Durston method remains the best way to do that.

    This is why you have to consider both the search space topology

    Sure. And the search space topology is extremely simple. The greater the different between two sequences, the greater the distance. Very simple, isn’t it? There is not much to be considered.

    Why is it so? Simply because variation is applied to the primary sequence. Variation happens randomly at DNA level. It has nothing to do with the protein. It has nothing to do with the phenotype. It’s only NS that “sees” the phenotype, not RV. Variation is a variation of sequence. The search space is a sequence space.

    and the nature of the search (i.e. localised/stepwise or random sampling)

    The nature of the search is clear. Neutral search that does not affect the function, or at least the folding, is localised (traversing the functional island). In no way it can explain new protein domains.

    Free neutral search, like in duplicated genes or non coding DNA, can search the whole space. It just needs time to get away from the initial state (not too much, indeed).

    Jump is possible, but limited to some forms of variation (such as frameshift mutation).

    The distribution of probabilities for achieving any particular state from a given point and in a given time are highly dependant on how your search proceeds and the shape of the landscape you are traversing.

    Sure. And that’s exactly what I have tried to analyze in detail.

  358. PaV:

    I absolutely agree. The role of transposons in primates is obvious, but it probably extends backwards.

    Another example is the rather sudden “origin” of the specific immune system in jawed fish, which is also attributed to transposon activity (with the appearance of the fundamental proteins RAG1 and RAG2: and no kidding here, human RAG1 is 1043 AAs long!)

  359. I don’t respond to “arguments” that I don’t understand, or that just don’t exist.

    Be more clear, and we’ll see…

  360. Hi there, gpuccio!

    Guys (Elizabeth, DrBot):

    First of all I want to thank you both for your intelligent contributions to this discussion. You are good interlocutors indeed.

    And thank you to you too :)

    While we catch our breath, I would like to add a couple of comments.

    Much confusion in your answers is, IMO, created by the fact that you refer to models and context that are completely different from what I am discussing (the origin of protein domains).

    Yes, I think so. I think a lot the disagreements on this site arise because we are “divided by a common language”, or by what linguists call “false friends” – we think we are talking about the same thing, but we are not!

    And one of the problems I keep trying to draw attention to is that it is often not clear whether we are talking about genotypes or phenotypes. It is the phenotype that has “fitness”, not the genotype. And in sexually reproducing organisms, the genes are independent, which is, again, important when discussing “drift”. In what follows you are clearly talking about genes and genotypes, and it is important to bear this in mind when trying to figure out where you are disagreeing with DrBot, who is talking about the fitness of phenotypes within “gene space”.

    The differences are many, but I would like to list briefly the most important:

    a) A protein domain is a functional unit, and a complex functional unit. The mean length of a protein domain is more than 100 AAs, but many are quite longer. A protein domain has a very specific biochemical function. This function is what must be considered first when we discuss the origin of domains. A protein domain, being a functional unit, cannot be decomposed in simpler functional units. Most protein domains are certainly well beyond conventional limit of 150 bits for the dFSCI in biological systems.

    And here I would disagree! We cannot consider “function” outside the context of the phenotype, and a gene for a protein doesn’t have a function unless that gene is expressed, and whether its function is beneficial, neutral, or deleteriouis for the phenotype will depend on the conditions under which it is expressed. And while a protein domain may not exist as such until a genetic sequence coding for it is generated, that doesn’t mean that a part-sequence can’t be a precursor of the whole. It’s just that, presumably, those part-sequences will be neutral with respect to the fortunes of the phenotype – so represent “flat” areas of the fitness landscape.

    If indeed they are not transferred, wholesale from viral sources, which is one important hypothesis.

    b) The infamous concept of “fitness function” is not good at all when speaking of protein domains. There is no simple or continuos fitness function that can be applied to that context.

    Yes, there is. Ignoring viruses for a minute, let’s take a sequence of base pairs that doesn’t code for anything, and a sequence of basepairs that codes for the simplest protein domain. And let’s assume that the protein, if it is made, does something useful for the organism. Any changes to the original sequence aren’t going to do much for the phenotype, so the fitness landscape in that “gene space” (or let’s call it “sequence space, as it isn’t really even a gene yet) is flat. Any change will result in no change in phenotypic fitness. Then it hits a protein domain. Bingo – leap in fitness. That’s a continuous function – sure it’s got a big step in it, but that doesn’t matter. What does matter is how big the plain is at the foot, which may be pretty big. Which is why the potential role of viruses is so intriguing.

    As we are discussing NS, the relationship between the specific biocemical function of a protein and the reproductive function can be very complex and indirect. That’s why, first of all, we must look at the biochemical function if the protein. That function must be present. It can be measured independently form the reproductive function. Therefore, we, as intelligent observers, can define and measure the biochemical function in precise and direct ways.

    Well, sure, but that’s after-the-fact. Once we have a protein that clearly does something to enhance reproductive success, however indirectly, then we have, by definition, a function that is “selected” (or, once present, highly conserved). What its function is may be of great interest, but from the point of view of biology, if it doesn’t help the organism reproduce, it isn’t functional at all, it’s a malfunction (however much fun it is for the organism).

    But NS can “see” the single protein, both positively and negatively, only in the measure that the specific biochemical function of that protein is fundamental for reproductive fitness.

    And I think you are getting into a muddle by trying to split function from reproductive success. NS doesn’t “see” anything, of course (and your scare quotes indicate that you know this, but perhaps you don’t know it quite deeply enough!). What we have is a protein that may or may not be expressed in a way that enhances the organism’s chance of reproductive success. If it doesn’t, its sequence is less likely to be conserved. If it does, it is more likely. And clearly if it isn’t produced at all, because the sequence doesn’t code for anything yet, then it won’t do anything, beneficial or otherwise, for the organism, except, possibly be a slight metabolic luxury.

    So, indeed, a mutation can be negative, or positive, in the biochemical sense, and still be invisible to NS.

    No. This makes no sense at all. You can’t consider “function” without considering the phenotype, and if a protein is made, or not made, and can do something, or not do something, or be expressed appropriately, or inappropriately for the phenotype, that cannot be “invisible to NS” because all “NS” is is differential reproductive success. And if the mutation has phenotypic effects and those phenotypic effects affect reproductive success, then that is NS. And if the new protein does nothing to affect the phenotype’s reproductive success as compared with a peer without the genetic ability to make the protein, then that protein doesn’t have a “function”. It’s just decoration.

    c) Protein domains are isolated islands of functionality. They have different structures and different functions.

    Well, they may be “islands” in the sense that on a fitness landscape they are buttes in a wide plain, but that doesn’t mean that they can’t be reached, because, as DrBot says, drift can carry populations across wide plains.

    Most of the experience in neutral evolution, so dear to Elizabeth, is derived form observation of the neutral evolution inside families. As I have already said in my previous post, that kind of evolution, although very important to assess relationships between species, doe not affect the function, or at most (but it can be debated, and is debated by Axe in his paper) could be repsonsible of small tweaks at the active site level, with changes of function but preservation of the general structure.

    Actually, it’s derived from fairly straightforward models! In which quite complex functional sequences can evolve, despite many necessary precursor steps being neutral with regard to the reproductive success of the phenotype. I do think you are being mislead by trying to consider “function” outside the context of the phenotype, and, specifically, outside the context of the fitness of the phenotype – its reproductive success.

    That kind of model does not apply to the generation of new domains, where a whole and completely new sequence of more than 100 AAs arises.

    Yes it does, because there is no reason to think that the sequence had no incremental precursors, even if we assume that they were not even semi-functional (which may not be the case). Although there is also the possibility that they evolved within viruses (which evolve much more rapidly) and actually did plonk themselves into the genome of cells. There’s at least some evidence IIRC that HGT and domain genesis ab initio, as it were, both contribute to the evolution of new domains. I’ll try to dig out the paper I read.

    For that kind of event, only three models can be conceived:

    *sucks teeth* Rash assertion! Never underestimate the number of models that can be conceived! What matters is how many make testable predictions that are subsequently supported!

    1) An existing, functional, transcirbed and translated gene gradually changes to a new gene. That is full of problems: fisrt of all the original function is rapidly lost, and it is not clear how NS would act, given the two different functions of A and B.

    An existing useful gene will tend to be highly conserved, so if by “functional” you mean “contributes to evolutionary success” yes indeed. That is in accord with DrBot’s model of the “ridge”.

    2) The process happens in a duplicated, inactivated gene. In that case, it is not clear how NS can act at all, and the variation remains by definition neutral. All the probability barriers apply.

    Except it turns out that, because of drift, those “probability barriers” are much lower than were once thought. An inactivated gene can still drift through the population, collecting mutations. This is why Behe’s IC notion just isn’t the barrier to evolution he thinks it is.

    3) The process happens in a segment of non coding DNA, possibly through transposon activity. All the probability barriers still apply, and NS cannot act (at least, not until a functional transcribed, translated protein does arise.

    Sure, but see above. Same possibility applies.

    My favourite model is definitely #3. That is the best model for design. And transposons are, at present, the best candidates for guided variation.

    Well, you’ve left out viruses. And you still have the burden of showing that the fitness landscape between functional domains is too wide and too featureless for probability to account for a route across it.

    Anyway, nice to talk to you again, will drop by in a bit in case you respond (I feel I’m departing UD like the Cheshire Cat, so I’ll leave you with a :D)

  361. Elizabeth:

    The problem here:

    Conversely, it may be that some proteins are Irreducibly Complex, in which case they are sitting on a high butte in a flat landscape. But again, that doesn’t mean they can’t be climbed, because as DrBot points out, populations can drift along horizontal ridges, and if they drift to the base of a bluff, there is nothing to stop them ascending to the top.

    is that this amounts to a “just-so” story told using the language of molecular biology.

    There are various parts to a protein sequence: you can have hydrophilic sections attached to hydrophobic sections, e.g., where the hydrophobic section sits in the cell membrane, while the hydrophilic section dangles outside, or inside of the cell.

    Likewise, there are “conserved” regions, and non-conserved regions—which easily translates into vital portions and less vital portions.

    Per se, neutral drift occurs in that portion of the protein sequence that is less vital. In the vital segments of the protein sequence, either positive, or negative selection is going to take place.

    So, yes, BOTH neutral drift and NS work side-by-side. And even in the highly-conserved (= vital) sections, a small amount of drift can, and does occur. And, it is possible for a previously “neutral” mutation to assume some kind of function. But all of this is very limited simply because the critical portions of proteins allow only the smallest amount of wiggle room (i.e., they’re “highly conserved”).

    What does this look like?

    Well, it means that if you change but ONE critical amino acid, then significant loss of function can occur; and if you change TWO critical amino acids, then death is likely to occur.

    IOW, there isn’t 12345; there’s, maybe, 123, with huge fall-offs associated with 3 versus 2, and even 2 versus 1.

    So you say that if you’re at the base of a “butte”, now all you have to do is scale it. Well, all you have to do to get to the next galaxy is travel faster than the speed of light. Sounds easy, doesn’t it. IOW, “scaling” the “butte” is the problem. And it’s a big problem for NS, let alone neutral drift.

    Behe worked with a mathematician by the name of Snoke to build a computer model of evolution that tried to simulate the model that evolutionary biologists proposed as explaining macroevolution: gene duplication, nuetral drift, selection, dah, dah, dah.

    Behe and Snoke constructed the model using assumptions highly favorable to Darwinian theory. Their results showed that evolutionary models were extremely limited, and that it would take huge amounts of generations to effect small changes.

    Based on comments he’s made here and there, I suppose he thought that his results were a little too pessimistic. So he decided to investigate further. The result was his study using the malarial parasite, and his Edge of Evolution. The parasite mutates randomly—call it a random walk, or call it neutral drift, whatever suits you—and it takes, in vivo, 10^20 replications to produce a new binding site consisting of a 2 amino acid change. These results are consistent with his computer model.

    So, at the end of the day, scaling “buttes” that involve changing more than ONE amino acid in the critical portion of a protein domain is almost impossible—either randomly, or even with selection in play.

    Certainly, to utilize simple models to help one envision difficult concepts can be worthwhile. But if the simplicity employed ends up being an over-simplification, then we’re more likely to confuse ourselves and others, than to produce anything that is helpful. As they say, “more heat, than light.”

  362. Elizabeth:

    The problem here:

    Conversely, it may be that some proteins are Irreducibly Complex, in which case they are sitting on a high butte in a flat landscape. But again, that doesn’t mean they can’t be climbed, because as DrBot points out, populations can drift along horizontal ridges, and if they drift to the base of a bluff, there is nothing to stop them ascending to the top.

    is that this amounts to a “just-so” story told using the language of molecular biology.

    I don’t know what people mean when they dismiss models as “just so” stories, PaV. I see it a lot, but I don’t understand it. I’m talking about testable hypotheses, not fairy tales that do not make testable predictions. Sure, it’s a metaphor, but it’s a very precise metaphor, and can be translated into real productive ouputs, as DrBot will attest.

    There are various parts to a protein sequence: you can have hydrophilic sections attached to hydrophobic sections, e.g., where the hydrophobic section sits in the cell membrane, while the hydrophilic section dangles outside, or inside of the cell.

    Likewise, there are “conserved” regions, and non-conserved regions—which easily translates into vital portions and less vital portions.

    Per se, neutral drift occurs in that portion of the protein sequence that is less vital. In the vital segments of the protein sequence, either positive, or negative selection is going to take place.

    I thought we were talking about the origins of a novel protein domain.

    But either way, what matters is the effect on the phenotype. Clearly if a sequence is “vital” it will be highly conserved, because no offspring bearing a lethal mutation to it will survive to pass on that lethal mutation.

    So, yes, BOTH neutral drift and NS work side-by-side.

    Well, I think it’s artificial to separate them, or, indeed to talk about “NS” in the same breath as “drift” anyway – “NS” is just a bias to the drift process. But as long as that’s what you mean, we agree.

    And even in the highly-conserved (= vital) sections, a small amount of drift can, and does occur.

    Meaning what? Yet again, it isn’t clear when you are talking about phenotype and when you are talking about gene! And if you are talking about a gene, then it matters whether you are talking about sexual or clonal reproduction. And also whether you are considering HGT. What do you mean when you say a “section” of a gene “drifts”? Do you mean it can accumulate minor variants and still be reproduced? Sure. And the “less vital” parts can accumulate more variation still be reproduced.

    And, it is possible for a previously “neutral” mutation to assume some kind of function.

    Yes indeed, by gene-gene interaction, but I’m not sure that’s what you mean. Perhaps you mean that it’s possible for a previously neutral phenotypic feature to become beneficial. Which is also true. But it’s important to distinguish between the two, as they are quite different.

    But all of this is very limited simply because the critical portions of proteins allow only the smallest amount of wiggle room (i.e., they’re “highly conserved”).

    Well, of course, but that’s looking from the evolved protein backwards, not from no-protein forwards. Once something has become useful, then you are right, there is less “wiggle room” – which is why gene duplication is probably an important process, and also HGT, in generating novel selectable phenotypic variance. But that’s OK, because we know that both those things happen, and that there is also some “wiggle room” (in other words there are functional variants of proteins) and also that sexual reproduction introduces yet another novelty-producing mechanism, namely recombination, whereby entire domains can be diced and spliced.

    What does this look like?

    Well, it means that if you change but ONE critical amino acid, then significant loss of function can occur; and if you change TWO critical amino acids, then death is likely to occur.

    Well, no, it doesn’t. But even if for some proteins it is true, then all it means is that those sequences will be highly conserved. And we know many sequences are. But being highly conserved after-the-fact is not the same as being vital before there is such a thing as the protein in the first place. Again, this is one of the many fallacies in Behe’s concept of Irreducible Complexity.

    IOW, there isn’t 12345; there’s, maybe, 123, with huge fall-offs associated with 3 versus 2, and even 2 versus 1.

    But you are travelling the wrong way. And I’m not quite sure, even what you are referring to. If you are talking about DrBot’s gene-space, the values are phenotypic fitness, and if there is a big “cliff” then that’s not a problem – the phenotypes will stick to the ridge.

    So you say that if you’re at the base of a “butte”, now all you have to do is scale it. Well, all you have to do to get to the next galaxy is travel faster than the speed of light. Sounds easy, doesn’t it. IOW, “scaling” the “butte” is the problem. And it’s a big problem for NS, let alone neutral drift.

    No, you are misunderstanding the metaphor. The “altitude” on DrBot’s fitness landscape is just that – fitness. You are confusing the height with the horizontal distance. What is difficult for a phenotype is getting across a plain, not scaling a cliff. Let’s say that it takes 10 neutral mutations to make a functional gene, but that functional gene confers a big reproductive advantage. The difficulty is getting across the “plain” represented by those 10 functional mutations, but once there are 9 in place, it is at the foot of the “butte”, and once it gets the 10th, up it goes.

    This is what I mean by it being important to get the metaphors straight, and to ensure we are talking about the same things when we use the same words! It’s so easy to think you are in disagreemente, when actually you are talking about quite different things!

    Behe worked with a mathematician by the name of Snoke to build a computer model of evolution that tried to simulate the model that evolutionary biologists proposed as explaining macroevolution: gene duplication, nuetral drift, selection, dah, dah, dah.

    Behe and Snoke constructed the model using assumptions highly favorable to Darwinian theory. Their results showed that evolutionary models were extremely limited, and that it would take huge amounts of generations to effect small changes.

    Well, no. It’s not my field, so I’m not in a position to evaluate it it, but if you are going to base your case on Behe & Snokes, then be aware of the limitations of their model, which the authors readily conceded in their response to the critique by Michael Lynch:

    Our paper (Behe and Snoke 2004) contains one simple result. When reasonable parameters are used with our model to estimate actual time scales or population sizes for the evolution of multi-residue (MR) protein features, they are unrealistically large. This implies that the model we chose, which is restricted to point mutations and assumes intermediate states to be deleterious, isn’t a plausible evolutionary pathway. One must therefore look about for a new model. We did not rule out such a possibility; in our original article, we explicitly stated, ‘‘we should look to more complicated pathways, perhaps involving insertion, deletion, recombination, selection
    of intermediate states, or other mechanisms, to account for most MR protein features.’

    PaV:

    Based on comments he’s made here and there, I suppose he thought that his results were a little too pessimistic. So he decided to investigate further. The result was his study using the malarial parasite, and his Edge of Evolution. The parasite mutates randomly—call it a random walk, or call it neutral drift, whatever suits you—and it takes, in vivo, 10^20 replications to produce a new binding site consisting of a 2 amino acid change. These results are consistent with his computer model.

    And, again, this has been extremely widely criticised. So only if the critiques can be countered, can you conclude anything from this.

    So, at the end of the day, scaling “buttes” that involve changing more than ONE amino acid in the critical portion of a protein domain is almost impossible—either randomly, or even with selection in play.

    Only if Behe is correct, and there have been plenty of critiques.

    Certainly, to utilize simple models to help one envision difficult concepts can be worthwhile. But if the simplicity employed ends up being an over-simplification, then we’re more likely to confuse ourselves and others, than to produce anything that is helpful. As they say, “more heat, than light.”

    Sure. But it is one thing to say that on principle, Irreducibly Complex things cannot evolve, when a simple model shows that they can, and another to show that this allegedly IC thing, or class of things could not have evolved, in which case your conclusion is only as good as your model, as Behe and Snokes themselves point out.

    And in any case model that aims to show that something “could not” happen is a very weak model, because at best you can conclude that your model is wrong, not that no comparable model is correct.

  363. Elizabeth:

    Nice contribution. But, obviously, I disagree.

    First of all, I don’t accept at all your constant reference to reproductive success as the only “function”.

    Biochemical functions are vwry well defined, and in themselves they have nothing to do with reproductive success.

    An enzyme is a perfect machinery to accelerate a specific chemical reaction. It does that, and accomplishes its function, whether in a living being or in the lab. It has a perfectly definable function.

    Many of those biochemical functions we use out of the context of the reproduction of living beings. Indeed, protein engineering is also about the possibility to have biochemical advantages from new molecules.

    So yes, I do keep the biochemical function of proteins separate form their phenotypic effect on reproduction.

    And anyway, I am still talking of phenotype. And enztme, the protein, is phenotype. Phenotype is not only reproduction. It is much more.

    Another statement that is, IMO, completely wrong is the following:

    Except it turns out that, because of drift, those “probability barriers” are much lower than were once thought.

    You don’t motivate that at all. It is not true. Drift does not change the probability barriers at all.

    Let’s go through it again.

    My original statement is:

    “The process happens in a duplicated, inactivated gene. In that case, it is not clear how NS can act at all, and the variation remains by definition neutral. All the probability barriers apply.”

    So, we are talking of a gene that is not translated, that can change freely. We are discussing the possibility that such a gene is the starting point for a different, unrelated protein domain of high complexity (more than 150 bits of dFSCI). We agree that all variation in that gene are, by definition, neutral (the gene is not translated). We agree that random genetic drift can happen.

    We agree, I hope, that for the new state to be reached the search must dare to go well out of the local (the state that should be reahced is unrelated at the sequence level).

    So I strongly state that, in this situation, all unrelated states have the same probability to be reached.

    Will you please explain why that should not be true, abd how drift should make the probability barrier lower?

    You go on affirming that. It is not true, and you have never explained why it should be so.

    Please, a clear and specific answer to that would be greatly appreciated.

    You say:

    An inactivated gene can still drift through the population, collecting mutations.

    It certainly can. But the probability of reaching a functional unrelated protein domain in that way is almost zero.

    The problem is not that such an achievement cannot be reached. For instance, if a designer guides the variation, it can certainly be reached, and even in a short time.

    On the contrary, with no guide, and by the effect of purely random variation, you need all the time of the universe to have a decent chance, even in a single case. Or more realistically, you cannot succeed even with all the time of the universe at your disposal.

    Well, you’ve left out viruses.

    Viruses are not autonomous replicators. Please, detail what your model about viruses is, and we will discuss it. But again, viruses use the already existing, complex resources of more complex beings.

    Even including viruses, however, the probability barriers cannot be matched. The higher replication rate of viruses can probably rise the probabilistic resources of a few orders of magnitude. But we in ID always keep tens of orders of magnitude of “buffer” in our analyses. No problem, even with viruses.

    you still have the burden of showing that the fitness landscape between functional domains is too wide and too featureless for probability to account for a route across it

    I have discussed that in detail many times. You must decide. If you are interested in that aspect (until now, you have usually avoided to discuss it), then we must go deeper into the concept of dFSCI and into the existing literature about protein function and the protein search space.

  364. You go on affirming that. It is not true, and you have never explained why it should be so.

    Please, a clear and specific answer to that would be greatly appreciated.

    Well, clearly I have not been clear, but I have certainly been specific! And, indeed, I have tried to explain.

    I’ll try again, but I probably won’t have time to get to this for a bit now. Thanks for your response anyway, and when I do get back, I’ll try to respond your whole post.

  365. EL:

    Sure, it’s a metaphor, but it’s a very precise metaphor, and can be translated into real productive ouputs, as DrBot will attest.

    In what ways is it productive?

    EL:

    Meaning what? Yet again, it isn’t clear when you are talking about phenotype and when you are talking about gene! And if you are talking about a gene, then it matters whether you are talking about sexual or clonal reproduction. And also whether you are considering HGT.

    Why add needless complications? The main distinction is between “highly conserved” regions of the protein’s gene sequence, and those parts that are not.

    EL:

    Yes indeed, by gene-gene interaction, but I’m not sure that’s what you mean. Perhaps you mean that it’s possible for a previously neutral phenotypic feature to become beneficial. Which is also true. But it’s important to distinguish between the two, as they are quite different.

    Why not simply talk about genotypes? Whether the fitness involves gene-to-gene interactions or whether it involves strictly phenotypic features doesn’t really matter than much when one is trying to talk about general principles. Yes, each might have it’s own special considerations, but the basic principles underlying the one or the other remains much the same. Again, why the needless complications?

    EL:

    Well, of course, but that’s looking from the evolved protein backwards, not from no-protein forwards. Once something has become useful, then you are right, there is less “wiggle room” – which is why gene duplication is probably an important process, and also HGT, in generating novel selectable phenotypic variance.

    Is this the spandrels of St. Mark’s here? Are we talking “exaptation”?

    If so, this is an example of a “just-so” type scenario.

    The problem with Darwinism is the lack of intermediates in the fossil record. The problem with neo-Darwinism is the lack of molecular intermediates: we don’t see them, but we’ll just assume they happened nevertheless.

    You quibble with Behe and Snoke’s paper. Well, here’s part of what they say in response to Michael Lynch’s criticism:

    “This is a strong requirement—that not only the end products, but steps along the way to a multiresidue function, must be either selected or at least neutral. Michael Lynch makes a similar assumption.

    Our model posited necessary intermediate mutations to be deleterious in the unduplicated gene; Lynch’s model assumes them to be neutral: ‘‘all 20 amino acids are equally substitutable in the intermediate neutral state’’ (Lynch 2005, this issue). All of his objections to our work stem from this difference.”

    This assumption on Lynch’s part seems to directly contradict what you just stated:
    Once something has become useful, then you are right, there is less “wiggle room”. Lynch allows all the wiggle room imaginable in the unduplicated gene.

    EL:

    But being highly conserved after-the-fact is not the same as being vital before there is such a thing as the protein in the first place. Again, this is one of the many fallacies in Behe’s concept of Irreducible Complexity.

    Here we go again with the miracle of “exaptation”! Has “exaptation” been “demonstrated”, or is it simply “assumed” to have happened? Where’s the proof?

    Or is it another “just-so” story once again?

    EL:

    If you are talking about DrBot’s gene-space, the values are phenotypic fitness, and if there is a big “cliff” then that’s not a problem – the phenotypes will stick to the ridge.

    Of course negative selection will keep them on what you call a “ridge”; but the pertinent question is how did it get up on that “ridge”?

    EL:

    You are confusing the height with the horizontal distance. What is difficult for a phenotype is getting across a plain, not scaling a cliff. Let’s say that it takes 10 neutral mutations to make a functional gene, but that functional gene confers a big reproductive advantage. The difficulty is getting across the “plain” represented by those 10 functional mutations, but once there are 9 in place, it is at the foot of the “butte”, and once it gets the 10th, up it goes.

    At last!! We’ve gotten to your notion of what happens in genomes!!

    I see now why you think Dawkins is so wrong. It’s because you think the brunt work of getting to new function is done by neutral mutations, not positive selection.

    And I have a metaphor for your scenario. It’s called: “Taking An Elevator Up Mount Improbable”! Or, as you Brits would say: “Taking A Lift Up Mount Improbable”!

    There’s two ways to go here. We can assess things without assuming the need for fixation of neutral mutations. And we can assess things assuming this isn’t necessary.

    In the first case, Kimura calculates that it takes around 3.5 million years for a SNP to become fixed for an effective population of 500,000. This has to happen 9 times given the example you’re using. So that’s 31.5 million yrs., simply to come up with a new functional gene. Isn’t that about the time of the entire Cambrian Explosion? This is way too slow.

    OTOH, assuming no fixation, then any individual organism/genotype with the first neutral mutation has to stay alive. If some deleterious mutation comes along anywhere else in the genome, then the organism dies, taking with it the needed mutation. So, negative selection is there all the time, weeding out the perhaps 100′s of deleterious mutations that occur during each replication. And this tightrope walk has to happen 9 times. Is this probable?

    Well, this looks like a “random walk” through a mine field.

    Next, consider this. The first neutral mutation can occur in any member of the population. But the second, the third, and so forth, mutations need to occur in the genome where the first occured since fixation isn’t assumed.

    So, how many of these “neutral mutations” will appear in the population? We have no idea. It could be zero; it could be a hundred, a thousand, we don’t know.

    But let’s say we’re dealing with a small number; let’s say a hundred. Then the probability of getting the second mutation at a specific spot is 1 in 10^9. This means that if the number of members of the population having the first mutation doesn’t increase, then it will take, on average, 10^7, or 10 million years to show up in those members having the first mutation. If you want to argue that during these 10 million years there will be other members of the population that will get the first mutation, then we also have to remember that during this same 10 million yrs. there will be members with the first mutation that will lose it. It’s this kind of back and forth flux that works into the notion of the time needed for fixation of a mutation. In this case, a fixation time less than 10 million yrs would be preferable. So, we have a time somewhere between 3.5 million yrs. and 10 million yrs.

    Again, this looks to be way too slow.

    But let’s say this is possible. Then shouldn’t we see “intermediates”? That is, shouldn’t we see some members of the population with 7 or 8 of the needed 9 neutral mutations? Well, where are they? Now our technology might not now be able to give us these answers, but I bet there are some studies done here and there that can even now give us hints as to whether or not we see these kinds of “intermediates”.

    To date, I haven’t heard of any such discoveries.

    So, here we have it: neutral drift is too slow, and positive selection is too costly (deadly–i.e., Haldane’s Dilemna = genetic load).

    EL:

    And, again, this has been extremely widely criticised. So only if the critiques can be countered, can you conclude anything from this.

    I’ve seen some of the critcisms, and have criticized some of the criticisms. And the criticisms in general amount to this: “It doesn’t take 10^20 replications to come up with just one new binding site, you can come up with quite a few!”

    Is this really a criticism? It sounds more like a capitulation.

    The other great big criticism is: “Where did Behe come up with 10^20 replications?!!!”

    Well, from a paper by someone working in the field. That’s why I included the words “in vivo” when discussing EofE, since, hypothetically, it should only take 10^16 replications; yet, in practice, the first a.a. substitution takes 10^12, and not 10^8 replications. The 10^20 figure is one that can be calculated from the known data. When a single infection of the parasite can produce upwards of10^10 parasites in one individual, and with millions of individuals infected each year, a mimimum figure for the required number of replications has to be around 10^13 to 10^15. And that many for what: 2 a.a. substitutions!!!!

    Ah, yes, Climbing Mt Improbable. In what, trillion upon trillions of years?

    EL:

    But it is one thing to say that on principle, Irreducibly Complex things cannot evolve, when a simple model shows that they can, and another to show that this allegedly IC thing, or class of things could not have evolved, in which case your conclusion is only as good as your model, as Behe and Snokes themselves point out.

    Behe and Snoke’s model wasn’t trying to demonstrate anything whatsoever about IC. They were simply trying to accurately model the evolutionary model then current.

    You’re “simple model” that “shows that [IC] things can [evolve]” involves propositions that have not been demonstrated, but simply assumed.

    OTOH, in Behe’s “Edge of Evolution”, nothing is assumed. It’s nature at work. I’d rather base my thinking on what nature is known to have done than on undemonstrated “assumptions”.

  366. a) NS, both negative and positive, seems to have no role, or only a really minor role

    b) Neutral variation can easily happen, and can easily reach any possible target

    Of course NS has a role – thats what EL and I keep saying – neutrality is DEFINED by NS acting on the search space. NS acts to keep a sequence neutral when there is no hill to climb but flat areas exist. Neutral variation cannot easily reach any target – how could a sequence of neutral mutations reach a target in the middle of a sea of deleterious function? They can’t because that, as a statement, makes no sense. By definition a move into deleterious function is not neutral!

    This is why you have to consider both the search space topology

    Sure. And the search space topology is extremely simple. The greater the different between two sequences, the greater the distance. Very simple, isn’t it? There is not much to be considered.

    Sorry but that is nonsense – Topology refers to the shapes of the surfaces in the landscape. What you are talking about is just the distances between two points. Consider these three examples:

    1 If there exists a series of steps from A to B, and each confers an advantage, then an evolutionary ‘search’ can ‘climb the hill’

    2 If there exists a series of steps from A to B, and each confers no advantage or disadvantage, then an evolutionary ‘search’ can ‘cross the ridge’

    3 If there exists a series of steps from A to B, and each is seriously harmful, then an evolutionary ‘search’ will never take more than one step in that direction.

    In the first two examples above the topology provides a navigable route from A to B, but not in example 3. Therefore the probability of getting from A to B in the three examples is different in each case (1 is the highest, 3 is the lowest) despite the distance between A and B being the same.

    Free neutral search, like in duplicated genes or non coding DNA, can search the whole space. It just needs time to get away from the initial state (not too much, indeed).

    No. You are still making the same cognitive error as before in viewing neutrality as different than selection. The sequence space includes sequences that code for proteins, that are not expressed, that are non coding and that are deleterious. Only those areas of the sequence space where a point mutation will not cause a change in selective potential are neutral, the rest are not – the rest are areas of sequence space upon which NS will act.

    The distribution of probabilities for achieving any particular state from a given point and in a given time are highly dependant on how your search proceeds and the shape of the landscape you are traversing.

    Sure. And that’s exactly what I have tried to analyze in detail.

    Ok, that is confusing because you said this above:

    The whole dFSCI barrier applies

    and previously you have been saying this:

    The problem is, if the system is only random, or mainly random, the probabilities are those relative to the whole dFSCI of each protein.

    and this:

    But now it is perfectly true that the search space can be freely traversed by NS, because there is no more the limit of negative selection, defending the functional island of A. It is true, as you say, that the initial variation will remain local, but as neutral variation accumulates, we are diving into the sea of unrelated states.

    And we can, now, reach B. But the probabilities are exactly those deriving from the total dFSCI of B. Or of the functional internediate, if and when it exists.

    Both of those statements are about the probabilities of getting from A to B using random sampling (or at best a random walk), not evolutionary search. They seem to assume that the entire search space is neutral with respect to fitness. The entire sequence space encompasses neutral, deleterious and advantageous areas, some of these areas do not form part of the searchable space – If you want to analyse the probabilities of getting from A to B in an evolutionary system you need to have a good understanding of the topology of the fitness landscape, you need to take into account how much of the sequence space is not searchable, how much of it is neutral, and how much of it confers some advantage. Just computing the distance from A to B tells you nothing in this regard.

    I think the error you seem to be making is in thinking that neutrality refers to a different search space than non neutral – it doesn’t, it is just a feature of the fitness landscape for the entire search space of the sequence. A neutral mutation does not render the entire search space neutral.

    If you have, for example, a duplication event, then a mutation to the duplicate will not destroy the function that exists in the original. The search space for the copy includes the existing function (a protein domain), other new functions (other protein domains), neutral and advantageous non coding sequences, non expressed sequences and deleterious sequences. The question here is whether there exists a route through sequence space for the duplicate from its starting state to a new functional state that does not require a move into deleterious function. Neutral moves don’t, and neither do moves into new advantageous functions of either a protein or non protein coding sequence.

  367. Natural selection does not act nor select.

    Not only that with AVIDA it has been demonstrated that once realiistic parameters are set your position looks like crap:

    The effects of low-impact mutations in digital organisms

    Chase W. Nelson and John C. Sanford

    Theoretical Biology and Medical Modelling, 2011, 8:9 | doi:10.1186/1742-4682-8-9

    Abstract:

    Background: Avida is a computer program that performs evolution experiments with digital organisms. Previous work has used the program to study the evolutionary origin of complex features, namely logic operations, but has consistently used extremely large mutational fitness effects. The present study uses Avida to better understand the role of low-impact mutations in evolution.

    Results:

    When mutational fitness effects were approximately 0.075 or less, no new logic operations evolved, and those that had previously evolved were lost. When fitness effects were approximately 0.2, only half of the operations evolved, reflecting a threshold for selection breakdown. In contrast, when Avida’s default fitness effects were used, all operations routinely evolved to high frequencies and fitness increased by an average of 20 million in only 10,000 generations.

    Conclusions:

    Avidian organisms evolve new logic operations only when mutations producing them are assigned high-impact fitness effects. Furthermore, purifying selection cannot protect operations with low-impact benefits from mutational deterioration. These results suggest that selection breaks down for low-impact mutations below a certain fitness effect, the selection threshold. Experiments using biologically relevant parameter settings show the tendency for increasing genetic load to lead to loss of biological functionality. An understanding of such genetic deterioration is relevant to human disease, and may be applicable to the control of pathogens by use of lethal mutagenesis.

    And if you have a duplication even then all you have is another protein diffusing through the organism ready to get in the way of important reactions.

  368. DrBot:

    Of course NS has a role – thats what EL and I keep saying – neutrality is DEFINED by NS acting on the search space. NS acts to keep a sequence neutral when there is no hill to climb but flat areas exist

    You are palying with words, and falling heavily into the trap of agency language, so feared by Elizabeth.

    You want to say that NS has the role of non existing when variationis neutral? that’s fine for me. What changes. The point remains that, if variation is neutral, it is not selected in any way.

    In the case of a non transcribed or non translated gene, the landscape is flat. No selection applies to the variation (more on that later).

    Neutral variation cannot easily reach any target – how could a sequence of neutral mutations reach a target in the middle of a sea of deleterious function?

    That’s exactly why existing functional genes don’t reach any distant target. Variation can occur only inside the functional island, or at most as minor tweaking at the active side level (as said many times).

    New genes are derived from non coding DNA, be it a duplicated non translated gene, or simply a repetitive sequence.

    Topology refers to the shapes of the surfaces in the landscape. What you are talking about is just the distances between two points.

    As said, in the case of a non active gene, the topology is simply flat. The distance remains the only pertinent topologic parameter.

    Instead, in the case of a functional gene, the topology is simply against any complex transition. Even separtated islands with the same function are impossible to reach, as shown in this paper about the ragged landscape model:

    “Experimental Rugged Fitness Landscape in Protein Sequence Space”

    A quote from the discussion:

    “In practice, the maximum library size that can be prepared is about 1013 [28,29]. Even with a huge library size, adaptive walking could increase the fitness, ~W, up to only 0.55.
    The question remains regarding how large a population is
    required to reach the fitness of the wild-type phage. The relative fitness of the wild-type phage, or rather the native D2 domain, is almost equivalent to the global peak of the fitness landscape. By extrapolation, we estimated that adaptive walking requires a library size of 10^70 with 35 substitutions to reach comparable fitness.”

    Get the idea?

    Your examples:

    1) If there exists a series of steps from A to B, and each confers an advantage, then an evolutionary ‘search’ can ‘climb the hill’

    OK. That is positive NS. Then there are intermediates. Then there are functional steps. Nothing of that is true for protein domains. Falsified.

    2) If there exists a series of steps from A to B, and each confers no advantage or disadvantage, then an evolutionary ‘search’ can ‘cross the ridge’

    It can, but it will not, because the proibabilities are too low. What do you think the dFSCI discussion is about? We are not talking of “possibility”, but of empirical credibility.

    3) If there exists a series of steps from A to B, and each is seriously harmful, then an evolutionary ‘search’ will never take more than one step in that direction.

    Agreed. That’s why functional genes remain as they are, and change only in sequence, while retaining their function. And so?

    Your error is in point 2. You attribute to neutral mutation a power it has not. Empirically.

    Therefore the probability of getting from A to B in the three examples is different in each case (1 is the highest, 3 is the lowest) despite the distance between A and B being the same.

    Yes, and in 2), that is the only alternative left to reach new unrelated domains, it is almost zero.

    So we know that darwinian evolution can wrok in a scenario that is not true, can maintain existing functions, and can never create new protein domains. That was my initial point, exactly.

    The sequence space includes sequences that code for proteins, that are not expressed, that are non coding and that are deleterious.

    Either I don’t understand what you are saying, or this is really nonsense.

    By what mechanism a sequence that is not expressed should be deleterious? Please, elucidate.

    Only those areas of the sequence space where a point mutation will not cause a change in selective potential are neutral, the rest are not – the rest are areas of sequence space upon which NS will act.

    Again, could you explain how a point mutation in a gene that is not expressed, or in non functional non coding DNA, could be non neutral, and dealed with by NS?

    The entire sequence space encompasses neutral, deleterious and advantageous areas, some of these areas do not form part of the searchable space

    All the space is searchable for non expressed sequences. Practically none of it is searchable for functional sequences, constrained by negative NS (except the functional island they are in).

    If you want to analyse the probabilities of getting from A to B in an evolutionary system you need to have a good understanding of the topology of the fitness landscape

    I have. And you?

    you need to take into account how much of the sequence space is not searchable, how much of it is neutral, and how much of it confers some advantage.

    I have discussed that.

    I think the error you seem to be making is in thinking that neutrality refers to a different search space than non neutral – it doesn’t, it is just a feature of the fitness landscape for the entire search space of the sequence. A neutral mutation does not render the entire search space neutral.

    No. Neutrality for an existing function is one scenario. As said, it creates constraint to change.

    Neutrality, instead, is the normal condition for variation in a non expressed, non functional sequence.

    They are two different scenarios, two different concepts.

    If you have, for example, a duplication event, then a mutation to the duplicate will not destroy the function that exists in the original. The search space for the copy includes the existing function (a protein domain), other new functions (other protein domains), neutral and advantageous non coding sequences, non expressed sequences and deleterious sequences.

    Exactly. The whole search space is neutral in that case, unless and until a new functional sequence is reached, transcribed and translated (and integrated in the existing scenario).

    The question here is whether there exists a route through sequence space for the duplicate from its starting state to a new functional state that does not require a move into deleterious function.

    Again the same error. No move is deleterious, until the sequence is translated. And no move is advantageous. You confound the potential advantage or damage in the genotipic sequence with a true phenotypic advantage (or damage).

  369. 57.2.3.3.2

    PaV,

    “I’d rather base my thinking on what nature is known to have done than on undemonstrated “assumptions”.”

    Absolutely. Behe keeps saying that (i) it is highly improbable rather than impossible (ii) the current evolutionary models are way to simple and, consequently, imprecise. In other words, just guesswork. As soon as the talk touches the details, their machinery grinds to a halt. With every next necessary mutation, probability plummets while complexity rockets up. But one thing that is certain is that neo-Darwinists do have fruitful imaginations.

  370. If you have, for example, a duplication event, then a mutation to the duplicate will not destroy the function that exists in the original. The search space for the copy includes the existing function (a protein domain), other new functions (other protein domains), neutral and advantageous non coding sequences, non expressed sequences and deleterious sequences.

    Exactly. The whole search space is neutral in that case, unless and until a new functional sequence is reached, transcribed and translated (and integrated in the existing scenario).

    If the whole search space for this gene is neutral then no mutation of any kind will cause the sequence to become deleterious or to become advantageous, to loose expression or gain it.

    You are basically saying that the gene can be anything – any possible gene – and it will not affect fitness because it is a duplicate. But then you say “unless and until a new functional sequence is reached” – this is a direct contradiction in terms. If the entire search space is neutral then by definition it contains NO advantageous functional sequences and NO deleterious ones.

    Now of course if you limit your enquiry to ONLY the parts of a sequence that do not control expression, and assume it is not expressed, then your entire search space from this frame of reference is neutral. What you have to remember is that the search space is ultimately for the whole genome, individual sequences can be viewed as sets of axis within that space. Changes from expression to non-expression are part of the space of possibilities therefore the search space is not flat with respect to fitness. A duplication event gives you two genes, one of which can potentially change without a loss of function (because the original retains the function) – the fitness landscape for the duplicate is defined in part by the fact that there is an identical sequence.

    Again the same error. No move is deleterious, until the sequence is translated. And no move is advantageous.

    Any unexpressed gene exists on a neutral area, yes. If a single mutation event will cause it to be expressed then it will step into an area of the search space where selection will operate.

    If you want to analyse the probabilities of getting from A to B in an evolutionary system you need to have a good understanding of the topology of the fitness landscape

    I have. And you?

    You are analysing the same search space and assuming that there are two different fitness landscapes – one neutral and one not. This is a major error!

  371. “You’re right that you absolutely cannot falsify someone’s belief that something is designed.”

    Therefore, ID is not science. It is a belief tacked onto science.

    You (intentionally?) spun my words. ID is not belief, it is the investigation of whether a phenomenon falls outside of the probabilistic resources of stochastic processes. If these can be empirically verified, the only other verified explanation left is design. Yes, I am restating the elementary definition of ID, but judging solely by this statement of yours, you do not grasp that yet.

    “ID is defeated in this instance (even though it actually was designed!) because the inference to the best explanation results in a probabilistically viable natural explanation.”

    Above, I reference a study showing a gene evolving by apparently natural processes, which are demonstrably random with respect to need. It creates a new functional protein. Is ID not defeated in this case because I’ve demonstrated a viable natural explanation for creation of new information? And secondly, where is the design inference? Is a long process, random with respect to need, comparable to human design?

    I am a mechanical engineer, not a biochemist; I do not want to pretend to be something I’m not. I have looked at that paper but not enough to have a really serious conversation with you. My initial thoughts were there were several point mutations along with the rearrangement of lots of repeat elements which contributed to the formation of multiple introns, yet no mention of possible step-wise selectability of any of these changes. And if it was all needed for end functionality, there would need to be a huge island of functionality for this to drift to as all of these changes would easily go way beyond the probabilistic resources of the universe if they were all necessary and the only options. Also, you seem to contradict yourself:

    24.1.1

    No evolutionary process can be exhaustively proven to be “blind and undirected.”

    45

    Above, I reference a study showing a gene evolving by apparently natural processes, which are demonstrably random with respect to need.

    We know that it took multiple point mutations as well as complex rearrangement of repeat elements, and we know of no step-by-step selection increases (so we’re assuming drift?) and don’t know of the size of the “island of functionality”, yet it is “demonstrably random”? I don’t see that demonstration. Please point it out to me if it is there (not being sarcastic).

    As I’ve said before, the design inference is without empirical support. Has anyone recorded the designer creating improbable amounts of information at once?

    We have plenty of empirical support of intelligence designing things, like this very comment. We do not have any evidence of a specific designer creating biological information. No ID advocate has asserted this (to my knowledge). So if someone is trying to use the design inference to prove the existence of the God of the Old Testament, then your argument is valid. If they are trying to use it to argue that at least some of life was designed, your argument means nothing. Analogy:

    ME: Someone murdered this man. It was no accident. See ______ as evidence.
    YOU: Do you have any evidence or direct observation of John Doe murdering him? If not then your inference is invalid.
    ME: I didn’t say that this evidence proves John Doe did it, just that someone did it, intentionally.

    Out of time, can’t get to the rest of your comment right now.

  372. DrBot:

    No. I am analyzing two different scenarios (evolution of a translated functional gene and evolution in a non translated duplicate or a non coning DNA sequence). It’s not an error at all.

  373. drBot:

    But then you say “unless and until a new functional sequence is reached” – this is a direct contradiction in terms.

    The contradiction is not mine. It is in the darwinist duplication model I am tentatively discussing. Not my fault. It’s the model that is inconsistent.

    In a design model, the inactive gene is prepared while remaining inactive, and only when it is ready, and everything else necessary has been prepared, it is shifted to translation.

    That is more or less what apparently happens in this case:

    “A Human-Specific De Novo Protein-Coding Gene Associated with Human Brain Functions”

    http://www.ploscompbiol.org/ar.....bi.1000734

  374. “In a design model, the inactive gene is prepared while remaining inactive, and only when it is ready, and everything else necessary has been prepared, it is shifted to translation.

    That is more or less what apparently happens in this case:
    63.1.2.1.2 gpuccio

    “A Human-Specific De Novo Protein-Coding Gene Associated with Human Brain Functions”

    http://www.ploscompbiol.org/ar…..bi.1000734″

    From the paper:
    “Insertion of repeat elements especially Alu contributed to the formation of the first coding exon and six standard splice junctions on the branch leading to humans and chimpanzees, and two subsequent substitutions in the human lineage escaped two stop codons and created an open reading frame of 194 amino acids.”

    So gpuucio, you believe that a process spanning millions of year, using mechanisms that are demonstrably random with respect to need, and that often cause disease and infertility is “intelligent design?”

    How did you determine this was a design process?

  375. By the way, I was the one who first presented that paper on this thread, over a week ago.

    I was curious if someone could calculate the gain in fciso for that de novo gene.

    Apparently not. This seems to be of no concern, and despite having quite tractable natural processed behind it, is now presented as an example of design.

    Remarkable.

  376. DrRec:

    By the way, I was the one who first presented that paper on this thread, over a week ago.

    I know. Thank you.

    So gpuucio, you believe that a process spanning millions of year, using mechanisms that are demonstrably random with respect to need, and that often cause disease and infertility is “intelligent design?”

    It could well be.

    And, obviously, the fact that transposons can behave randomly does not demonstrate that they always behave randomly. The same for mutations.

    How did you determine this was a design process?

    I didn’t. The following steps are missing:

    a) Confirmation and isolation of the protein

    b) Identification of its structure and biochemical function.

    If the protein is confirmed and analyzed, the desisn inference can be made, based on the dFSCI of the protein.

    I was curious if someone could calculate the gain in fciso for that de novo gene.

    You have already computed the maximum dFSCI: 20^194 (if I remember well). The reald dFSCI is more difficult here, because it is a new protein, and the Durston method cannot be applied (it applies to protein families).

    An analysis of the structure funtion relationship of the specific protein could help.

  377. DrBot:

    No. I am analyzing two different scenarios (evolution of a translated functional gene and evolution in a non translated duplicate or a non coning DNA sequence). It’s not an error at all.

    It is a major error, and the fact you can’t see it is even more worrying!

    What is the difference between a translated gene sequence and a non translated gene sequence or just a sequence?

    The search space for a sequence includes anything that the sequence can be – all possible configurations. Some of those configurations produce proteins, others will not get translated. Fitness is the result of the sequence being in a specific configuration within the context of the whole genome and the environment.

    A gene sequence that is not expressed is not a search space, it is a specific configuration, a specific sequence. The search space is an n dimensional hypercube that incorporates an entire genome. Remember, gene sequences can vary in length so a search space for just a single gene has a variable number of dimensions and they are just a set of sub dimensions within the whole genome. Within that search space there may be many sequences that are not expressed, but also many that are.

    In a design model, the inactive gene is prepared while remaining inactive, and only when it is ready, and everything else necessary has been prepared, it is shifted to translation.

    That is very revealing in terms of the designers methods. The gene is taken ‘off line’ within an extant population and then adjusted via a sequence of steps before being re-activated.

    One could draw a few inferences from that.
    Firstly, the designer was not capable, or did not want, to make all the changes at once – if all the changes could have been made at once then there would be no need to take the gene off line.

    Secondly it indicates that members of the extant population were the only available entities in which to make these adjustments. In terms of observed design processes the normal approach would be to use a sandbox for development and testing before updating the actual system with the completed and tested new functions.

    It also indicates that the designer had some reason, or restriction in their operation, that required them to prepare the gene over such a long time period.

    If you think about it in terms of microsoft working on updates for windows:

    Normally Microsoft will have a set of test computers in their HQ, locked away from public view, and will use them for preparing and testing software patches. They will then publish the update. All the computers running windows will get the update – they will go from one version of a function to the new version in one step.

    What you are saying is the equavalent of microsoft loggin in to other peoples computers and tweaking the code directly and gradually over many years, then not testing it in any kind of sandbox but just switching the new function on when they think it is ready.

    That is more or less what apparently happens in this case:

    What emperical evidence have you got of the gene being intentionally prepared – how did the interactions between the designer and the organism occur?

  378. What you are saying is the equavalent of microsoft loggin in to other peoples computers and tweaking the code directly and gradually over many years, then not testing it in any kind of sandbox but just switching the new function on when they think it is ready.

    You have to give the Designer credit for coming up with a process that is empirically compatible with mainstream biology. I have to apologize for using the word “poof” to describe the process.

    I might point out that in the reality we observe, the beta test code is online, and has actual effects on fitness.

  379. In a design model, the inactive gene is prepared while remaining inactive, and only when it is ready, and everything else necessary has been prepared, it is shifted to translation.

    But that makes no sense, gpuccio. Genes are switched on and off throughout the lifetime of the organism. If they weren’t we wouldn’t be differentiated multicellular creatures able to function in response to our environment. Every second of your life, genes are being activated and deactivated in your body, in different places, and in response to different inputs.

    “Frontloading” is a brave concept, but it’s falsified by even a cursory glance at what genes actually do. And proteins in themselves are neither good not bad; what matters (from an evolutionary PoV) is whether they are expressed in a manner that enhances the reproductive success of the phenotype. A protein expressed by a gene in one part of the body, or at one time in development, may be highly beneficial; the same gene expressed later, or earlier, or elsewhere, may be highly deleterious. Or neutral.

    This is why it simply makes no sense to talk about evolutionary processes without reference to the phenotype. It’s like saying “let’s not complicate things by looking the left side of the equation, let’s just concentrate on the right hand side”.

    (This response is partly to PaV as well, but I’ll try to get back later to be more specific).

  380. Elizabeth:

    I am afraid you are really making a great confusion here. Genes are activated or deactivated all the time, that is true, but not in the sense that they are no more functional genes. The mechanisms of temporary activation or deactivation in individual transcriptomes are part of a complex regulatory network. They have nothing to do with the genes becoming non functional and no more appropriate for translation.

    A duplicated gene can become non functional in may different ways. A very simple event can be the appearance of stop codons in the gene, that interrupt transcription.

    I quote from Wikipedia:

    “The duplication of a gene results in an additional copy that is free from selective pressure. One kind of view is that this allows the new copy of the gene to mutate without deleterious consequence to the organism. This freedom from consequences allows for the mutation of novel genes that could potentially increase the fitness of the organism or code for a new function.”

    So, the idea is, the duplicated gene in this model is not a gene that is transitorily non transcribed in a specific cell type. It is a gene that has become non coding in whole species, and for long evolutionary times. That’s exactly what gives it the chance to accumulate free mutations, by definition “neutral”.

    But not certainly the power to overcome probabilistic barriers.

    As DrBot has correctly pointed out, other problems remain: if the gene is not translated, how can NS “realize” at phenotypic level that some functional sequemce has been reached?

    I don’t know, and really don’t care. The model is bogus.

    But gradual remodeling of a non coding sequence, followed by a final repristination of its translation, is a very good model for design.

    And why do you go on saying that I am not referring to the phenotype? I am always referring to the phenotype. But, as I have said, the phenotype is not only reproductive fitness. It is a lot of other things.

    A functional protein ia a functional item in the phenotype, whethet it affects reproductive fitness or not.

    A non functional protein is non functional. Period. It cannot implement any function. Sometimes it can be detrimental, but not always.

    A non functional protein coding gene always implies a non functional protein, or the absence of a functional protein. We must reason on the whole system: genotype, biochemical phenotype, and all other levels of phenotype, including reproductive fitness. All are interrelated.

  381. Me: “So gpuucio, you believe that a process spanning millions of year, using mechanisms that are demonstrably random with respect to need, and that often cause disease and infertility is “intelligent design?”

    “It could well be.”

    Unless you can demonstrate it IS, ID is just theistic evolution with a bad guess.

    “And, obviously, the fact that transposons can behave randomly does not demonstrate that they always behave randomly. The same for mutations.”

    LOL. Non-uniformity isn’t the greatest thing in science, but when your science believes in miracles, guess you gotta go for it.

    “You have already computed the maximum dFSCI: 20^194 (if I remember well). The reald dFSCI is more difficult here, because it is a new protein, and the Durston method cannot be applied (it applies to protein families).”

    Ahh, see gpucio is too honest! Where others just cite the maximum dfisco, he realizes that is the calculation for the maximum! So what would the actual calculation be? Durston has an estimate, based on the number of sequences found in nature that perform the same function. (Of course, in this case there is only 1.)

    Taking known sequences with the same function substantially lowers the fits, to the point functional proteins and enzymes are below the some probability thresholds set here.

    But even that is just an estimate! Nature hasn’t explored all of sequence space, and no one can make the entire sequence space of a protein and measure function.

    So you’ve got an estimate at best behind your ‘design inference.’

    Which is odd, because in the same post you say: “the desisn inference can be made, based on the dFSCI of the protein.”

    And how would you do that calculation again!?!

    You also have a circular non-falsifiability to it. I present something that has loads of what you call fisco, that developed over millions of years in processes known to be random with respect to need. Apparently natural. BUT, if it does have fscio, it is designed. See the problem?

  382. DrRec:

    See the problem?

    No.

  383. LOL.

    “the desisn inference can be made, based on the dFSCI of the protein.”

    Which you admit can’t reasonably be calculated. Estimated, maybe.

    And if it could, any process, no matter what the mechanism, that exceeds the value you set, makes it designed. ANY potential falsification, by definition then=design.

    No problem there?

  384. DrREC:

    DrREC: So gpuucio, you believe that a process spanning millions of year, using mechanisms that are demonstrably random with respect to need, and that often cause disease and infertility is “intelligent design?

    gpuccio: “It could well be.”

    DrREC:Unless you can demonstrate it IS, ID is just theistic evolution with a bad guess.

    Have you ever had a cellphone go bad, DrREC? Would you then conclude that it wasn’t designed?

    You’re sneaking in theological considerations here, evident in your conclusion that ID is just “theistic evolution”.

    If you want to talk theology, then do you want to talk about the reality of the devil? Do you want to talk about what the devil is able to do, or not do?

    If God can change an amino acid, can the devil?

    In the gospels we have Jesus talking about a woman who had a bleeding ulcer, and saying that it was the “devil” who had kept this daughter of Israel in this bondage for twenty years. So, if you want to talk theology, we can talk theology. But, otherwise, let’s not just assume that only perfection is permissible in a world created by God. Revelation has a lot to say about all of this. God’s foolishness is wiser than man’s wisdom. That’s just a sample.

  385. No religion. Just design. ID is based on inference to human design.

    I would say the following are not properties of human design:

    Utilizing mechanisms that are random with respect to need.
    Utilizing mechanisms that are open ended (no timeline) and not goal oriented.
    Utilizing mechanisms as likely to be deleterious to the design as beneficial.

    You’re the one that jumped on the bad design=theology argument. Showed your hand there.

    By the way, I didn’t think dualism (even in lighter forms) was popular these days. Burning at the stake and internal crusades and inquisitions and all…..

  386. Elizabeth:

    I don’t know if you’ve looked at my response to your response on page 2? But let me pick out just this one point since I think it demonstrates quite clearly where we disagree.

    Any changes to the original sequence aren’t going to do much for the phenotype, so the fitness landscape in that “gene space” (or let’s call it “sequence space, as it isn’t really even a gene yet) is flat. Any change will result in no change in phenotypic fitness. Then it hits a protein domain. Bingo – leap in fitness. That’s a continuous function – sure it’s got a big step in it, but that doesn’t matter. What does matter is how big the plain is at the foot, which may be pretty big.

    FIRST:

    I can see why you disagree with Dawkins. You see no direction whatsoever in the biochemical changes taking place in the DNA template. For you, everything is neutral drift—until it isn’t anymore (for selection now “selects”—excuse the “agency” language).

    SECOND:

    Your scenario should, I think, be called: “Taking A Lift Up Mount Improbable”. Or, for Americans, “Taking An Elevator Up Mount Improbable”. It’s almost like magic. Which should give everyone pause.

    THIRD:

    While you talk about “how big the plain is at the foot”, with, apparently the larger the plain the better, you don’t apply a time-frame to this traverse; nor do you deal with deleterious mutations that are occurring far more frequently than anything called ‘beneficial’. The larger (longer) the plain, the more time that will be needed; and the more opportunity, therefore, for harmful mutations to disrupt any possible future function.

    In my retort on page 2, I do a calculation demonstrating the importance of “fixation”—the importance of which you refuse to acknowledge. I invite you to take a look at that calculation. It’s at 57.2.3.3.2.

  387. “It’s almost like magic. Which should give everyone pause.”

    ?

  388. That was supposed to be a backwards question mark-indicator or irony.
    Guess U+2E2E isn’t supported here.

  389. DrREC:

    Design is a logical inference. We see the hallmarks of design, and we infer design.

    This is far different than saying I can make a rabbit appear out of thin air.

  390. DrREC:

    I would say the following are not properties of human design:

    Utilizing mechanisms that are random with respect to need.
    Utilizing mechanisms that are open ended (no timeline) and not goal oriented.
    Utilizing mechanisms as likely to be deleterious to the design as beneficial.

    Excuse me. Aren’t you the one who wants to point out the utility of evolutionary algorithms as useful in other fields of human endeavor?

    By the way, I didn’t think dualism (even in lighter forms) was popular these days. Burning at the stake and internal crusades and inquisitions and all…..

    You’ve showed your hand!

  391. Umm, PaV, you really seem to be struggling with this whole topic.

    Humans don’t implement, as final solutions, designs that include modifications of an earlier design that are random with respect to need or impede an earlier function.

    What we do is implement systems that use stochastic variation and methods of automatically assessing functionality as a tool for generating final solutions.

    Unlike nature, we are only interested in the end result – if you are using a GA to design a circuit board you don’t implement every design, only the best one you have generated at the end of the process.

  392. A functional protein ia a functional item in the phenotype, whethet it affects reproductive fitness or not.

    A non functional protein is non functional. Period. It cannot implement any function. Sometimes it can be detrimental, but not always.

    The only test of functionality is reproductive success. Recall the infamous study of “rescue” by “randomly” generated protein sequences. The exact nature of the rescue was not understood.

    Explain how a designer knows — absent selection — what the effect of a new sequence will be.

  393. Petrushka:

    The only test of functionality is reproductive success.

    ???? That is really big! So, I suppose, if I test the enzymatic activity of a protein in the lab, I am not testing a functionality?

    The exact nature of the rescue was not understood.

    But it could certainly be understood. Reproductive success is just one of all the functions that can be defined.

    Explain how a designer knows — absent selection — what the effect of a new sequence will be.

    First of all, a designer can well use selection: intelligent selection.

    And secodnly, it is perfectly possible to know in advance the effect by a thorough understanding of biochemical laws (that is the concept of top down protein engineering. It’s not easy, but it can be done).

  394. DrBot:

    Yes, I’m struggling to try and understand your contentions—which, thus far, seem entirely unfounded.

    Arrogantly, you fail to see that the designs in nature surpass those of mere humans.

    Do you see this?

    How many times have we read in the paper that scientists were designing this, that or the other, based on the way that nature has solved the problem.

    What you also fail to see is that human design, indeed, has one goal in mind. OTOH, the Designer’s goal is design something that can adapt to differing environments. Hence, different “solutions”, if you will, are necessitated at different moments of time dependent on a whole hosts of variables. With such requirements, a certain open-endedness is unavoidable, and necessary.

    Now, can we claim that this is entirely so? No. But can the fact that “seeming” imperfections and adaptive dead-ends disprove the role of a Designer? Again, the answer is no.

    This is why, in posing the question to gpuccio, his answer was: “It could well be.”

  395. DrBot:

    No religion. Just design. ID is based on inference to human design.

    I let this go the first time; but since you want to take an aggressive tack, then let’s talk about this a little bit.

    ID is NOT based on inference to “HUMAN” design; it’s based on an inference to “DESIGN”.

    The level of sophisticated programming evident in the eukaryotic cell is completely beyond anything a human designer can come up with—and, likely, could ever come up with (We’ll see about that one down the line). Hence, we’re dealing with a designer that far surpasses our intellects—humbling as that might seem to some.

    It is nothing but an intellectual distraction to claim that without our “human” experience of design and designers, this “inference” could not otherwise be made, and, that, therefore, ID can ONLY infer to a human design, and no more.

    This is pure silliness, as becomes evident when considering SETI, for example, which attempts to detect signs of an intelligence outside of our world that might easily (if not presumably) be “higher” than our own.

    IOW, to say that the design inference must be limited to what human designers can do, that otherwise we’re impotent to detect it, is a bogus claim.

    In sum, your statement that ID is based on inference to human design is completely off the mark.

  396. 68.1.2.1.4 PaV

    “ID is NOT based on inference to “HUMAN” design; it’s based on an inference to “DESIGN”.”

    I can only conclude that you don’t know what an inference is. What other design have we observed as a basis of this inference?

    Even this site disagrees with you: “Moreover, ID satisfies all the conditions usually required for scientific inquiry (i.e., observation, hypothesis, experiment, conclusion):

    “It is based on empirical data: the empirical observation of the process of human design, and specific properties common to human design…..”
    http://www.uncommondescent.com/faq/

    “This is pure silliness, as becomes evident when considering SETI, for example, which attempts to detect signs of an intelligence outside of our world that might easily (if not presumably) be “higher” than our own.”

    But SETI performs the search looking for halmarks of intelligent signals, based on what we think those would be from a human perspective.

    “In sum, your statement that ID is based on inference to human design is completely off the mark.”

    What is an inference, and what is the observation ID is based on, if not to human design?

    By the way, you could remove “human” from my post, and preserve the meaning. Those are not discernable indicators of design. Period.

  397. First: Is DrREC also DrBot? This gets a little confusing.

    So, I’ll assume DrREC is not DrBot.

    I can only conclude that you don’t know what an inference is. What other design have we observed as a basis of this inference?

    And I can only conclude that your not careful about making proper distinctions.

    To make an inference “to human design” is to infer that humans are responsible for the design of life; which, of course is preposterous.

    Perhaps DrBot (DrREC?) meant to say “ID is based on what we know of human design”, or, “ID is based on inference from human design”.

    As to the quote from the UD website, it says that ID is based on “the empirical observation of the process of human design, and specific properties common to human design.” Does this anywhere say that it is based on an “inference to human design”? No.

    But SETI performs the search looking for halmarks of intelligent signals, based on what we think those would be from a human perspective.

    This, really, is quite cheeky. Revelation tells us that we’re made in the image of God. It would then be quite proper to understand our faculty of reason as being similar to that of God’s. Thus, the “hallmarks” of human design can be reasonably taken to be similar to how God designs. (In fact, if one traces the whole history of modern science, it stems from an understanding of inertia inferred from the Biblical accounts of Creation. You might want to consult Stanley Jaki’s “The Savior of Science.”)

    But what reason have you to believe that human reason—leaving God and creation out of this for the moment—can be projected onto alien life forms (should they exist)?

    Further, if you believe that you can project these “hallmarks of intelligence” onto creatures you know nothing of, then this is to say that these “hallmarks” can be understood in an abstractly. And if they can be abstracted, then what prevents anyone from projecting, or detecting, them when it involves an unknown designer?

    ID posits that cellular organisms display all of the “hallmarks” of intelligent agency. It’s not an “inference to human design”. It’s a scientific view that vastly different life-forms are best explained by the guiding hand of intelligent design—scientific in the very same sense as forensic science.

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