Home » Irreducible Complexity, News » Mike Behe: A Blind Man Carrying a Legless Man Can Safely Cross the Street

Mike Behe: A Blind Man Carrying a Legless Man Can Safely Cross the Street

(11 January 2012) Here

The work of Finnegan et al (2012) strikes me as quite thorough and elegant. I have no reason to doubt that events could have unfolded that way. However, the implications of the work for unguided evolution appear very different to me then they’ve been spun in media reports. ( http://tinyurl.com/7lawgpl ) The most glaringly obvious point is that, like the results of Lenski’s work, this is evolution by degradation. All of the functional parts of the system were already in place before random mutation began to degrade them. Thus it is of no help to Darwinists, who require a mechanism that will construct new, functional systems. What’s more, unlike Lenski’s results, the mutated system of Thornton and colleagues is not even advantageous; it is neutral, according to the authors. Perhaps sensing the disappointment for Darwinism in the results, the title of the paper and news reports emphasize that the “complexity” of the system has increased. But increased complexity by itself is no help to life — rather, life requires functional complexity. One can say, if one wishes, that a congenitally blind man teaming up with a congenitally legless man to safely move around the environment is an increase in “complexity” over a sighted, ambulatory person. But it certainly is no improvement, nor does it give the slightest clue how vision and locomotion arose.

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139 Responses to Mike Behe: A Blind Man Carrying a Legless Man Can Safely Cross the Street

  1. One thing I really appreciate about Dr. Behe very much is that where the Darwinists tried to hide their failure to empirically validate their pet theory with actual evidence by using the art of obfuscation to obscure the results, Dr, Behe, on the other hand, has a gift for making complicated ideas readily accessible for the general public to understand in clear no nonsense terms:

    A Blind Man Carrying a Legless Man Can Safely Cross the Street – Michael J. Behe – January 2012
    Excerpt: Finnegan et al’s (2012) work intersects with several other concepts. First, their work is a perfect example of Michael Lynch’s idea of “subfunctionalization”, where a gene with several functions duplicates, and each duplicate loses a separate function of the original. (Force et al, 1999) Again, however, the question of how the multiple functions arose in the first place is begged. Second, it intersects somewhat with the recent paper by Austin Hughes (2011) in which he proposes a non-selective mechanism of evolution abbreviated “PRM” (plasticity-relaxation-mutation), where a “plastic” organism able to survive in many environments settles down in one and loses by degradative mutation and drift the primordial plasticity. But again, where did those primordial functions come from? It seems like some notable workers are converging on the idea that the information for life was all present at the beginning, and life diversifies by losing pieces of that information. That concept is quite compatible with intelligent design. Not so much with Darwinism.,, Finally, Thornton and colleagues latest work points to strong limits on the sort of neutral evolution that their own work envisions.,,,
    http://behe.uncommondescent.co.....he-street/

  2. I wonder what GCU will have to say about Behe’s findings?

    After all it was GCU who brought it to the table first.

  3. I’d like to ask Dr. Behe how he figures common descent happened if mutations don’t add new molecular machines (which he admitted to in his book) and/or new anatomical features…(or even parts of them.)

  4. vh, you may be able to ask Dr. Behe personally at ENV. His post is there and, though monitored, the comments are open.

  5. vh: Common descent can have happened if all those molecular machines were there from the “beginning” (whatever that is, but corresponding to the Cambrian explosion). Anything occuring after that is rearrangement and degradation of pre-existing materials and possibilities. In that case Common Descent is independent of the method of origin. Front-loading.

  6. In Chapter 10 of The Edge of Evolution, “All the World’s a Stage”, there is a section titled, “No Interference” (which begins on p. 229 in my edition) in which Behe gives us a kind of parable that explains his idea of how common descent and design could both be true.

  7. I posted the following on the comments section of Behe’s DI blogpost, we’ll see if they are brave enough to post it.

    Dr. Behe concludes,

    Finally, Thornton and colleagues latest work points to strong limits on the sort of neutral evolution that their own work envisions. The steps needed for the scenario proposed by Finnegan et al. (2012) are few and simple: 1) a gene duplication; 2) a point mutation; 3) a second point mutation. No event is deleterious. Each event spreads in the population by neutral drift. Notice that the two point mutations do not have to happen together. They are independent, and can happen in either order. Nonetheless, this scenario is apparently exceedingly rare. It seems to have happened a total of one (that is, 1) time in the billion years since the divergence of fungi from other eukaryotes. It happened only once in the fungi, and a total of zero times in the other eukaryotic branches of life. If the scenario were in fact as easy to achieve in nature as it is to describe in writing, we should expect it to have happened many times independently in fungi and also to have happened in all other branches of eukaryotes.

    These are pretty baffling statements. Duplications in the membrane-ring part of the V-ATPase and its relatives (A-ATPase, F1Fo-ATPase) are, I believe, fairly well-known. It’s been awhile since I looked at it, but google things like “duplication proteolipid”, chloroplast c-subunit Fo-ATPase, etc. It’s not exactly rare, certainly not the only known event.

    Furthermore, cases of what are obviously duplicated-and-modified parts in “molecular machines” are absolutely ubiquitous. Fully half of the core flagellum proteins (those of the rod, hook, and filament) can be accounted for this way. Various cilia have various duplicated tubulins, dyneins, etc. Similarly for blood-clotting and the adaptive immune system.

    Duplication-and-divergence doesn’t explain everything that we want to know about the origin of the large number of “required” protein parts that make up “molecular machines”, but it successfully explains a large part of it. Basically, it ain’t no fair for ID advocates to go around shouting from the rooftops that “Darwinism can’t explain how system X has Y different required proteins, nyah nyah nyah!” and then pretend like it’s no big deal at all when it looks like something like Y/2 “required” parts of your average “molecular machine” can be accounted for by the “no big deal” duplication-and-divergence mechanism. If producing new required parts is “no big deal”, then the whole “lots of proteins are required, gradual evolution can’t produce this” argument is a lot less convincing.

    (The duplication-and-divergence mechanism, by the way, long well-accepted within science by anyone who knew anything; the Thornton lab’s recent work just reconstructs a particular instance in amazing detail.)

    But, by all means, the more ID advocates keep moving goalposts, the better. It didn’t work in Dover and it won’t work in science.

  8. His post on UD is not, however, open for comments.

  9. If producing new required parts is “no big deal”, then the whole “lots of proteins are required, gradual evolution can’t produce this” argument is a lot less convincing.

    One simple question.

    Behe has this to say about Thornton’s work, with emphasis added:

    “The most glaringly obvious point is that, like the results of Lenski’s work, this is evolution by degradation. All of the functional parts of the system were already in place before random mutation began to degrade them.

    Are you saying Behe is incorrect in the statement quoted above? And I want to stress: I’m not asking “Do you think Behe is wrong about anything else.” I mean, specifically, is he wrong about the portion I quoted above?

    Thank you.

  10. NickMatzke is still confused as ID is not anti-evolution and using duplicated and modified parts is engaging in question-begging.

    Keep humping that strawman Nick, it must make you feel important. Unfortunately it makes you look impotent…

  11. nick

    if we need to go from ttss to flagellum, we need a new protein.

    look at this paper :

    http://www.ncbi.nlm.nih.gov/pm…..PMC211289/

    in this case is the flagellin protein(part of the flagellum tail).

    its minimal length need 310 amino acid. no less.

    the sequance space for 310 aa is minimum 2^310!

    the protein cannt evolve from a simpler protein because its the minimum and the researcher get a invalid protein after they cut out near 190 amino acid

    so how can we get to flagellum from ttss?

    secondly, if you need only a 2 mutation to get a new function, and the first one is neutral, you need somthing like 7^10 fixation event, we need more of the age of the earth.

  12. 7^10 =10^7

  13. 7^10 =10^7

    Hmm, no, those are not equal.

    Okay, you were probably saying that there was a mistake in the prior comment, and what was written as 7^10 should have been written as 10^7.

    I’m just commenting that, taken literally, your equation is false.

  14. Behe, and all you ID guys, rely on an arbitrary and continuously-changing definition of “degradation”. When parts are lost, that’s “degradation”. When parts are gained (as here), *that’s* degradation. When binding site specificity increases, that’s called degradation, since the generality and versatility of the ancestral binding site has been reduced. But when binding site specificity *decreases*, that’s *also* called degradation, since loss of specificity must be degradation. When bacteria adapt to resist antibiotics, that’s “evolution by degradation”, since typically antibiotic-resistant mutants have a fitness cost compared to nonresistant bacteria in an antibiotic-free environment. But if a bacterium loses some genes and grows faster as a result, that’s *also* degradation, since genes were lost.

    Ditto for “information”, “specified complexity”, etc. It’s all just a word game used to avoid the evidence for evolution. But practically every adaptation in biology involves the “degradation” of something else. Bird wings have a “fitness cost” just like antibiotic resistance mutations, and flying ability is often lost in predator-free environments on islands. The evolution of the tetrapod jaw involved the loss of the functionality of gills. Etc.

    Word games like this are just cheap excuses for not dealing with the actual evidence, they are not serious responses to the data.

  15. I’ve been itching to say that all day, but I knew you’d say it better :)

  16. Yes, he is wrong. These are not degrading, just changing. Mutations can result in improvement in the probability of reproducing, reduce the probability, or have no effect. If the change improves the probability of reproducing it is more likely to become prevalent than the original form, but not guaranteed. Similarly, drift can result in even a neutral change to become prevalent in the population. But it is very unlikely, but not impossible, for a negative change to become prevalent.

    All DNA does is code for the arrangement of amino acids, no more, no less.

  17. its minimal length need 310 amino acid. no less.

    And you know this exactly how? You have a link to research that has explored all possible histories?

  18. And all possible histories to all possible flagella?

    And all possible histories to all possible motility systems?

  19. It’s really amazing how the history of god of the gaps argument repeats itself. First there were no transitional fossils, then as transitional fossils were found there were gaps, then as gaps were filled we had punctuation, then as punctuation was explained the whole argument starts over with genomes.

    Which is why Thornton et al is the current enemy. How dare he actually test whether cousin sequences can be linked by a common ancestor sequence.

  20. Hey Nick- can a company lose money of each sale and make it up on volume, ie selling more?

    The following offers the argument pertaining to anti-biotic resitance:

    Is Bacterial Resistance to Antibiotics an Appropriate Example of Evolutionary Change?

    But all that is moot because you are still stuck on the silly strawman that ID is anti-evolution- hump that baby NickM!

    BTW how can we test the premise that the tetrapod jaw involved the loss of functionality in the gills? Can we mutate the heck out of fish embroys and see that?

  21. Nick states:

    It’s all just a word game used to avoid the evidence for evolution.

    How deeply twisted and Ironic of you to state that Nick, because neo-Darwinists, of which you yourself are a prime example, are engaged full force in deceptive word games (obfuscation) to make it appear as if evolution (atheistic/materialistic neo-Darwinian evolution that is) has any substantiating evidence at all.

    Moreover If you want to falsify ID, Michael Behe (that would be Doctor Michael Behe to you!) lays out a very simple criteria right here:

    Michael Behe on Falsifying Intelligent Design – video
    http://www.youtube.com/watch?v=N8jXXJN4o_A

    Myself, instead of the pathetically low hurdle that Dr. Behe required, I would demand that neo-Darwinists ‘randomly evolve’ a molecular machines, or novel functional protein folds, from scratch, repeatedly, so as to establish Darwinian grand claims ‘scientifically’:

    i.e. In spite of the fact of finding molecular motors permeating the simplest of bacterial life, there are no detailed Darwinian accounts for the evolution of even one such motor or system.

    “There are no detailed Darwinian accounts for the evolution of any fundamental biochemical or cellular system only a variety of wishful speculations. It is remarkable that Darwinism is accepted as a satisfactory explanation of such a vast subject.”
    James Shapiro – Molecular Biologist

    The following expert doesn’t even hide his very unscientific preconceived philosophical bias against intelligent design,,,

    ‘We should reject, as a matter of principle, the substitution of intelligent design for the dialogue of chance and necessity,,,

    Yet at the same time the same expert readily admits that neo-Darwinism has ZERO evidence for the chance and necessity of material processes producing any cellular system whatsoever,,,

    ,,,we must concede that there are presently no detailed Darwinian accounts of the evolution of any biochemical or cellular system, only a variety of wishful speculations.’
    Franklin M. Harold,* 2001. The way of the cell: molecules, organisms and the order of life, Oxford University Press, New York, p. 205.
    *Professor Emeritus of Biochemistry, Colorado State University, USA

    Michael Behe – No Scientific Literature For Evolution of Any Irreducibly Complex Molecular Machines
    http://www.metacafe.com/watch/5302950/

    “The response I have received from repeating Behe’s claim about the evolutionary literature, which simply brings out the point being made implicitly by many others, such as Chris Dutton and so on, is that I obviously have not read the right books. There are, I am sure, evolutionists who have described how the transitions in question could have occurred.” And he continues, “When I ask in which books I can find these discussions, however, I either get no answer or else some titles that, upon examination, do not, in fact, contain the promised accounts. That such accounts exist seems to be something that is widely known, but I have yet to encounter anyone who knows where they exist.”
    David Ray Griffin – retired professor of philosophy of religion and theology

    Well Nick, despite all your bluster, there are no new molecular machines to show for your beloved theory, how about just a single novel functional protein fold???

    Estimating the prevalence of protein sequences adopting functional enzyme folds: Doug Axe:
    Excerpt: The prevalence of low-level function in four such experiments indicates that roughly one in 10^64 signature-consistent sequences forms a working domain. Combined with the estimated prevalence of plausible hydropathic patterns (for any fold) and of relevant folds for particular functions, this implies the overall prevalence of sequences performing a specific function by any domain-sized fold may be as low as 1 in 10^77, adding to the body of evidence that functional folds require highly extraordinary sequences.
    http://www.ncbi.nlm.nih.gov/pubmed/15321723

    Proteins Did Not Evolve Even According to the Evolutionist’s Own Calculations but so What, Evolution is a Fact – Cornelius Hunter – July 2011
    Excerpt: For instance, in one case evolutionists concluded that the number of evolutionary experiments required to evolve their protein (actually it was to evolve only part of a protein and only part of its function) is 10^70 (a one with 70 zeros following it). Yet elsewhere evolutionists computed that the maximum number of evolutionary experiments possible is only 10^43. Even here, giving the evolutionists every advantage, evolution falls short by 27 orders of magnitude.
    http://darwins-god.blogspot.co.....d-not.html

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

    Shoot Nick, though you never will admit it, you ain’t even in the right ballpark to begin with with the materialistic neo-Darwinian framework. 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)

    etc.. etc.. etc..

  22. Nick,

    I asked a pretty simple question, and I asked it fairly. That it provoked a whole lot of hand-waving and bluster doesn’t encourage me.

    Behe, and all you ID guys,

    I’m not an “ID guy”, and you know it. I don’t think ID is science, though admittedly that position is tied to my not thinking anti-ID is science either. I asked my question because if Behe was wrong about what he said, I wanted to know why.

    rely on an arbitrary and continuously-changing definition of “degradation”. When parts are lost, that’s “degradation”. When parts are gained (as here), *that’s* degradation. When binding site specificity increases, that’s called degradation, since the generality and versatility of the ancestral binding site has been reduced. But when binding site specificity *decreases*, that’s *also* called degradation, since loss of specificity must be degradation.

    “Parts are gained here”, Behe claims (if I understand him), in the sense that a cellular machine capable of performing tasks A, B and C was started with. This machine was duplicated, and eventually you ended up with three machines that only did A, only did B, and only did C. This really does not seem to challenge anything Behe has discussed.

    Furthermore, your understanding of Behe seems flawed here. It’s not that gaining parts must mean degradation, and losing parts must mean degradation, and more specificity must mean degradation, and less specificity must mean degradation. If you “gain a part” by copying the machine such that drift and selection causes it to lose functionality (Likewise for “become more specified”) because mutations made it incapable of doing anything else, that’s degradation. If you “lose a part” because mutations have rendered some parts incapable of functioning or lost altogether, that’s degradation. If your machine “becomes less specified” because its ability to limit what it applies to relies on a part that becomes broken by mutation, that’s degradation. (Example: ‘I can only get through this door if I have the right keycard. But if I smash the lock, anyone can get through.’ I think it’s fair to call this an example of degradation.)

    Word games like this are just cheap excuses for not dealing with the actual evidence, they are not serious responses to the data. Sorry for stealing that from you, but holy hell, it applies to you a hell of a lot more than it seems to apply to Behe here. I gave you a chance – I asked you a fair question, utterly bereft of culture-warriorisms, Behe-cheerleading, or otherwise. Your response was to rant, blow smoke and – frankly – try to BS people. Not good.

  23. It’s not a word game, nullasalus. That you think it is is a measure of the communication problem here.

  24. Nick Matzke:

    Furthermore, cases of what are obviously duplicated-and-modified parts in “molecular machines” are absolutely ubiquitous. Fully half of the core flagellum proteins (those of the rod, hook, and filament) can be accounted for this way.

    Umm, that the rod proteins in the flagellum can be accounted for by gene duplication doesn’t mean that this is how they arose. Thus, although the rod proteins FlgBCFG share sequence similarity with each other, this doesn’t imply gene duplication per se. There is always the possibility of convergent evolution at the molecular level accounting for this sequence similarity.

  25. It’s not a word game, nullasalus. That you think it is is a measure of the communication problem here.

    It’s not a communication problem. It’s an actual disagreement – they exist, you know – in this case, borne out of Matzke making it sound as if gaining parts, losing parts, gaining specification and losing specification are all instances of degradation according to ID proponents, when (at least in Behe’s case) what’s being argued is that how parts are gained, how they are lost, etc, is what matters.

    I have an extremely low opinion of your intellectual honesty, and I have no interest in wasting my time with you. You said Matzke said what he did better than you could have – I agree. How about leaving this task to your better?

  26. Which is why Thornton et al is the current enemy. How dare he actually test whether cousin sequences can be linked by a common ancestor sequence.

    I know, right? Why can’t Behe be appreciative of Thornton and company, right? Why can’t he say something like this guy:

    “I never thought it would happen but, in my estimation, Richard Lenski has acquired a challenger for the title of “Best Experimental Evolutionary Scientist.” Lenski, of course, is the well-known fellow who has been growing E. coli in his lab at Michigan State for 50,000 generations in order to follow its evolutionary progress. His rival is Joseph Thornton of the University of Oregon who, by inferring the sequences of ancient proteins and then constructing (he calls it “resurrecting”) their genes in his lab, is able to characterize the properties of the ancestral proteins and discern how they may have evolved into more modern versions with different properties.”

    Or maybe this:

    “The work of Finnegan et al (2012) strikes me as quite thorough and elegant.”

    Why can’t ID proponents talk about people’s ideas like this, rather than treating them as the enemy?

  27. bornagain77,

    What’s with the triple commas?

  28. 28

    Not enough detail, eh? We’ve heard that before.
    http://ncse.com/book/export/html/2520

    Please give us the equally detailed and well-tested ID explanation for the origin of the vertebrate immune system.

  29. 29

    null,

    After years and years of seeing people drag out the “it’s just degradation!” excuse in a multitude of self-contradictory ways, without the slightest bit of reflection on rigorously defining what distinguishes “degradation” from “improvement”, I figured I would point it out.

    Behe’s supposed challenge to evolution was about how you get systems with multiple required parts. It was supposed to be hard for evolution to produce systems with multiple required parts, because a system missing the part is “by definition nonfunctional” and couldn’t be preserved by evolution. The Thornton lab’s article demonstrates one way you can increase the number of required parts. As I said in my first comment, it doesn’t explain everything, but it is clear that the duplication-and-divergence mechanism explains a lot of the required parts in these various systems. This is a huge point against Behe’s claim.

  30. 30

    Umm, that the rod proteins in the flagellum can be accounted for by gene duplication doesn’t mean that this is how they arose. Thus, although the rod proteins FlgBCFG share sequence similarity with each other, this doesn’t imply gene duplication per se. There is always the possibility of convergent evolution at the molecular level accounting for this sequence similarity.

    Um, not really. Known cases of sequence convergence are rare and typically limited to a handful of amino acids, or to very weak/vague sequence similarities. Gene duplication is overwhelmingly the more common and more likely explanation for decent amounts of sequence similarity. Gene duplication produces a copy of a sequence. Copying gives you the similarity.

    This is even more true in the case of the flagellum axial rod, where we already have various examples of multiple flagellin proteins in a single genome, etc. (the “classic” Salmonella just has one, but many bacteria don’t follow the classic pattern), some of them specialized for different structural functions (e.g. another hook-flagellin linker protein).

    The gene duplication explanation is obvious, plausible, and simple, and matches everything we already know about molecular mechanisms and their commonality. The “convergence” explanation, in this case, is desperate special pleading with no support except for wishful thinking by ID fans.

    Let me give you a hint — you would have a better chance of arguing that the rod/hook family and the flagellin+linker family have independent origins. The homology evidence is much weaker there. But within each family, it’s rock solid, you can easily bring it up on any BLAST search.

  31. Nick to show others how dishonest you, and your cohorts at the NCSE (National Center for Selling Evolution), are I reference this:

    “A Masterful Feat of Courtroom Deception”: Immunologist Donald Ewert on Dover Trial – audio
    http://intelligentdesign.podom.....1_03-08_00

    In this following podcast, Casey Luskin interviews microbiologist and immunologist Donald Ewert about his previous work as associate editor for the journal Development and Comparitive Immunology, where he realized that the papers published were comparative studies that had nothing to do with evolution at all.

    What Does Evolution Have to Do With Immunology? Not Much – April 2011
    http://intelligentdesign.podom.....9_03-07_00

    The blatant deception, from neo-Darwinists at Dover, did not stop with immunology;

    The NCSE, Judge Jones, and Bluffs About the Origin of New Functional Genetic Information – Casey Luskin – March 2010
    http://www.discovery.org/a/14251

    Materialists/Atheists like to claim evolution is indispensable to experimental biology and led the way to many breakthroughs in medicine, Yet in a article entitled “Evolutionary theory contributes little to experimental biology”, this expert author begs to differ.

    “Certainly, my own research with antibiotics during World War II received no guidance from insights provided by Darwinian evolution. Nor did Alexander Fleming’s discovery of bacterial inhibition by penicillin. I recently asked more than 70 eminent researchers if they would have done their work differently if they had thought Darwin’s theory was wrong. The responses were all the same: No.
    Philip S. Skell – (the late) Professor at Pennsylvania State University.
    http://www.discovery.org/a/2816

    Podcasts and Article of Dr. Skell
    http://www.evolutionnews.org/2.....40981.html

    Darwinian Medicine and Proximate and Evolutionary Explanations – Michael Egnor – neurosurgeon – June 2011
    http://www.evolutionnews.org/2.....47701.html

    Intelligent Design and Medical Research – video
    http://www.metacafe.com/w/7906908

    In fact, as to the somewhat minor extent evolutionary reasoning has influenced medical diagnostics, it has actually led to much ‘medical malpractice’ in the past:

    Evolution’s “vestigial organ” argument debunked
    Excerpt: “The appendix, like the once ‘vestigial’ tonsils and adenoids, is a lymphoid organ (part of the body’s immune system) which makes antibodies against infections in the digestive system. Believing it to be a useless evolutionary ‘left over,’ many surgeons once removed even the healthy appendix whenever they were in the abdominal cavity. Today, removal of a healthy appendix under most circumstances would be considered medical malpractice” (David Menton, Ph.D., “The Human Tail, and Other Tales of Evolution,” St. Louis MetroVoice , January 1994, Vol. 4, No. 1).

    “Doctors once thought tonsils were simply useless evolutionary leftovers and took them out thinking that it could do no harm. Today there is considerable evidence that there are more troubles in the upper respiratory tract after tonsil removal than before, and doctors generally agree that simple enlargement of tonsils is hardly an indication for surgery” (J.D. Ratcliff, Your Body and How it Works, 1975, p. 137).

    The tailbone, properly known as the coccyx, is another supposed example of a vestigial structure that has been found to have a valuable function—especially regarding the ability to sit comfortably. Many people who have had this bone removed have great difficulty sitting.
    http://www.ucg.org/science/god.....-debunked/

    Darwinian evolution is simply useless, indeed a hindrance, to science;

    Science Owes Nothing To Darwinian Evolution – Jonathan Wells – video
    http://www.metacafe.com/watch/4028096

  32. further note:

    Falk’s fallacy – Feb. 2010
    Excerpt: This (the immune system) is one of the most amazing processes ever described.,,, Whatever may be said about it, it is a highly regulated, specified, directed and choreographed process. It is obviously the product of overwhelmingly brilliant design,,,
    http://www.uncommondescent.com.....ks-falacy/

    Response to Kathryn Applegate – Caroline Crocker PhD.- cell biologist and immunologist – October 2010
    Excerpt: Diversity of antibodies generated by B cells is due to deliberate, cell-engineered changes in the DNA sequence, not random mutations. In fact, I have never before heard the process whereby functional antibodies are formed (before they encounter antigen) described as mutation. And it is well-known that the appearance of functionality as a result of a mistake-mutation is extremely rare. Of course, after encountering antigen the hypervariable regions of the antibody DNA do undergo somatic hypermutation, but again this is in particular places and is controlled by enzymes.,,,
    http://www.uncommondescent.com.....more-15176

    Generation of Antibody Diversity is Unlike Darwinian Evolution – microbiologist Don Ewert – November 2010
    Excerpt: The evidence from decades of research reveals a complex network of highly regulated processes of gene expression that leave very little to chance, but permit the generation of receptor diversity without damaging the function of the immunoglobulin protein or doing damage to other sites in the genome.
    http://www.evolutionnews.org/2.....40661.html

  33. Nick,

    After years and years of seeing people drag out the “it’s just degradation!” excuse in a multitude of self-contradictory ways, without the slightest bit of reflection on rigorously defining what distinguishes “degradation” from “improvement”, I figured I would point it out.

    Yeah, Nick – do you realize that you can “improve” something while degrading it in the relevant sense? That these are not exclusive terms? Behe himself, in the very article quoted, alludes to this – he’s stated it explicitly before, on multiple occasions. Not to mention that in Thornton’s case, he doesn’t think that what took place was a case of “improvement” in a selection sense.

    Don’t think you can get out of this one by complaining that you’re criticizing some supposed lack of rigor on the part of ID proponents – there was no contradiction here or no Behe’s behalf pointed out by you, certainly not from myself. I asked you straight up whether Thornton’s case was one of acquiring ‘multiple parts’ by degradation, as Behe claimed. It seems the answer was “yes”, but since “yes” sounds bad, we had to get the usual Matzke bluff and fury which amounted to ‘These ID people think that if a cellular machine loses parts due to mutations, it’s degradation! But they ALSO think that if a cellular machine is copied and errors accumulate so both copies now can only do 1/2 of the functions they originally did, that that too is degradation! Look how ****ing slippery they are! It’s as if they think BOTH cases are examples of degradation – how can that be!?’

    Behe’s supposed challenge to evolution was about how you get systems with multiple required parts. It was supposed to be hard for evolution to produce systems with multiple required parts, because a system missing the part is “by definition nonfunctional” and couldn’t be preserved by evolution.

    No, Nick. Behe’s supposed challenge was not merely ‘How do you get multiple parts?’, full stop. It had and has to do with irreducibly complex systems, such that removing those parts meant the system could no longer function as it was. The “If I bust apart a mousetrap, I can make a stupid tie clip!” answer to Behe wasn’t a relevant reply to him in the past, and the “If you start with a cellular machine capable of performing multiple discrete functions, duplicate it, then break different parts of the machine, you get two machines that don’t do the same thing insofar as they each only do 1/2 of what the original machine already could do” reply isn’t accurate now. And what’s more, you goddamn know it.

    Word games like this are just cheap excuses for not dealing with the actual evidence, they are not serious responses to the data.

  34. Nick Matzke:

    Um, not really. Known cases of sequence convergence are rare and typically limited to a handful of amino acids, or to very weak/vague sequence similarities. Gene duplication is overwhelmingly the more common and more likely explanation for decent amounts of sequence similarity. Gene duplication produces a copy of a sequence. Copying gives you the similarity.

    The key phrase here is “known cases.” There have been few extensive investigations on the pervasiveness of convergent evolution at the molecular level. There is,of course, the study by Gareth Jones, “Molecular Evolution: Gene Convergence in Echolocating Mammals.” However, a more impressive paper on the subject came out in 2010. In a paper entitled “Adaptive molecular convergence: Molecular evolution versus molecular phylogenetics,” by Castoe et al., the authors found significant cases of molecular convergence in 13 mitochondrially-encoded proteins of lizards and snakes. I don’t think you can really call this a case of a “handful of amino acids” or “very weak/vague sequence similarities.”

    So, the point here is that significant convergent evolution at the molecular level isn’t all that implausible. Unfortunately, as of this date (AFAIK), no real research has been made to investigate the pervasiveness of molecular convergence among bacterial genomes.

    Anyways, I’ve been up all night long exploring some sequence stuff with FlgBCEFGK, so I won’t make my main case here yet. Suffice it to say that, interestingly, when the Salmonella rod proteins FlgE and FlgK (a cladogram generated by ClustalW suggests that they are more closely related to each other than to the other rod proteins)are aligned using ClustalW, the sequence identity (~15%) isn’t all that impressive. Of course, when we BLAST these proteins and find that they share sequence similarity along with significant E-values, the possibility that they are indeed related by gene duplication is quite strong. Nevertheless, we shouldn’t dismiss that possibility of convergent evolution since a case may be made for it. By the way, the percentage of identical codons per identical amino acid residues in sequence alignments of these proteins is basically what we would expect under the convergence hypothesis. Just saying.

    So, basically, the key point of my little essay is: don’t rule out molecular convergence since research shows that this can quite plausibly occur.

    Now I’m off to catch a wink of sleep, and I probably won’t respond until my little adventures with FlgBCEFGK sequences are completed.

  35. petrushka

    the link is broken or somthing. try “minimal size of flagellin” in google

    from the article:

    Various deletions were introduced into the central region of Escherichia coli flagellin (497 residues) without destroying its ability to form flagellar filaments. The smallest flagellin retained only the N-terminal 193 residues and the C-terminal 117 residues, which are suggested to be the domains essential for filament formation.

    J Bacteriol. 1988 July; 170(7): 3305–3309

    if you read the paper you can see that after they cut smoe amino acid the flagellin become invalid

    elizabeth

    yes,they fail to do that.if an half of protein is useless,how can you get to a full protein?

  36. By using gene duplications Nick Matzke is engaging in question-begging.

    By refusing to understand taht ID is not anti-evolution Nick Matzke is engaging in wilfull ignorance.

    By thinking that by getting the components you can get the proper assembly configuration Nick matzke is relying on imagination.

  37. I suggest you do some PSI-BLAST searches with it here:

    http://blast.ncbi.nlm.nih.gov/.....lastSearch

    I suggest you restrict the search to the Swissprot database to save cluttering up the page. You will find the homology to FlgG and FlgE by the second iteration and to FlgF by the third iteration.

    Similar considerations apply to flagellins and hook proteins, where the length of the surface-exposed central domain is highly variable.

  38. notes as to Starbuck’s post:

    “One fact in favour of the flagellum-first view is that bacteria would have needed propulsion before they needed T3SSs, which are used to attack cells that evolved later than bacteria. Also, flagella are found in a more diverse range of bacterial species than T3SSs. ‘The most parsimonious explanation is that the T3SS arose later,” Howard Ochman – Biochemist – New Scientist (Feb 16, 2008)

    Phylogenetic Analyses of the Constituents of Type III Protein Secretion Systems
    Excerpt: We suggest that the flagellar apparatus was the evolutionary precursor of Type III protein secretion systems.
    http://www.horizonpress.com/jmmb/v2/v2n2/02.pdf

    I am convinced that the T3SS is almost certainly younger than the flagellum. If one aligns the amino acid sequences of the flagellar proteins (that have homologous counterparts in the T3SS), and if one also aligns the amino acid sequences of the T3SS proteins, one finds that the T3SS protein amino acid sequences are much more conserved than the amino acid sequences of the flagellar proteins. There are two possible explanations for this: (1) The T3SS is younger than the flagellum, or (2) The T3SS proteins are under more functional constraints than flagellar proteins, and so the sequences in T3SS proteins cannot diverge as much. We may rule out option #2 in the light of both in vitro and in silico mutagenesis. For example, I performed an in silico alanine scan on flagellar proteins and their T3SS homologues using SNAPs and found that flagellar proteins are under more functional constraints than T3SS proteins.
    (E.g., ~39% of the positions in FliF result in a non-neutral mutation when an in silico alanine scan is performed, ~34% of the positions in YscJ result in a non-neutral mutation — YscJ is FliF’s T3SS homologue, for those of you who do not know).
    http://www.uncommondescent.com.....ent-389250

    Indeed? Consider the facts:
    The flagellar proteins are all longer than the T3SS proteins, with the exception of FliN (YscQ is the only T3SS protein that is longer than its flagellar homologue). Further consider that the flagellar proteins have a higher degree a “functional specificity” than their T3SS counterparts. By this I mean that, in order for the flagellar proteins to carry out their function, very specified amino acid residues need to be in the proteins. This is not true of T3SS proteins: T3SS proteins seem to be capable of tolerating more amino acid substitutions than flagellar proteins. The implication of this? Namely, very specific mutations would not be needed for the T3SS proteins to carry out their function. T3SS proteins are generally less stable than their flagellar counterparts, yet they can still carry out their function. Let’s just take a look at one example of how it is very plausible for a T3SS protein to evolve from its flagellar homologue:
    FliF is ~550 amino acid residues in length, while its homologous counterpart (YscJ) is ~270 amino acid residues in length. Obviously, FliF has an extra ~200 residues because those residues are required for flagellar function, but those extra residues are NOT required for YscJ to function. A simple deletion event of those ~200 residues would result in the YscJ function. Yet, to get from YscJ to FliF would require very specific mutations, because those ~200 residues are rather specific and need to be specific in order to carry out the flagellar function. “A gene duplication followed by very specific amino acid substitutions would be needed to get from YscJ –> FliF, yet a simple deletion event would be needed to get from FliF –> YscJ.” So, not-very-specific mutations are needed to get from a flagellum to a T3SS.
    Incidentally, I should like to know what new binding sites would have to evolve in order to get from flagellum to T3SS — I do not deny that new binding sites can evolve, I am just curious about this.
    And, of course, I accept the idea that new information can arise through mindless processes.

    In conclusion: while the evolution of a T3SS –> flagellum would require very specific mutations, the evolution of flagellum –> T3SS could be accomplished by just a few, not very specific mutations.
    http://www.uncommondescent.com.....ent-389432

    A Darwinian mechanism for the origin of the flagellum is not the only explanation for homology. Just take a look at the sequences designed by Fisher et al. If one aligns those designed, un-evolved sequences, one finds that they are homologous to each other. In short, designed sequences can also result in homology. In light of this, sequence homology can hardly be explained only by Darwinian mechanisms.
    References:
    Fisher et al. “De Novo Designed Proteins from a Library of Artificial Sequences Function in Escherichia Coli and Enable Cell Growth.”

    Firstly, I think I’ve already sufficiently demonstrated exactly why it’s plausible for the T3SS proteins to evolve from their flagellar homologues, but it is less plausible for flagellar proteins to evolve from their T3SS counterparts. While a single truncating mutation would be sufficient for YscJ to evolve from FliF, a fairly large number of very specific mutations would have to occur for FliF to evolve from YscJ. Indeed, it certainly seems like there is no real obstacle to a flagellum à T3SS evolution, and just some truncating mutations would be needed for the T3SS proteins to evolve from their flagellar homologues (and, of course, some mutations would follow that would improve the overall T3SS structure, stabilizing it, etc.).

    That said, I will now point out where I think your argument is lacking in rigor:
    Do T3SS have highly conserved functional regions and binding sites? Yes, but here’s why it’s perfectly plausible for those features of T3SS to evolve, while it is not quite so plausible for those features to evolve in the flagellum. If the T3SS evolved from the flagellum, it would evolve with the binding sites that were in the flagellar proteins (unless a function evolved from the flagellum that did not require binding sites). In other words, the T3SS didn’t evolve any new binding sites – it just ‘inherited’ the binding sites that were present in the flagellum. The same argument is true, of course, for highly conserved functional regions et al. The conclusion? To my knowledge, no new binding sites or highly conserved functional regions would have to evolve in order for the T3SS to evolve from the flagellum.,,,

    Incidentally, given that the modern T3SS is definitely not ancestral to the flagellum, you are left without any evidence as to where FliF, FliP, FliM, etc., might have come from.
    http://www.uncommondescent.com.....ent-389603

    further notes:

    Bacterial Flagellum – A Sheer Wonder Of Intelligent Design – video
    http://www.metacafe.com/watch/3994630

    Bacterial Flagellum: Visualizing the Complete Machine In Situ
    Excerpt: Electron tomography of frozen-hydrated bacteria, combined with single particle averaging, has produced stunning images of the intact bacterial flagellum, revealing features of the rotor, stator and export apparatus.
    http://www.sciencedirect.com/s.....220602286X

    Electron Microscope Photograph of Flagellum Hook-Basal Body
    http://www.skeptic.com/eskepti.....gure03.jpg

    Engineering at Its Finest: Bacterial Chemotaxis and Signal Transduction – JonathanM – September 2011
    Excerpt: The bacterial flagellum represents not just a problem of irreducible complexity. Rather, the problem extends far deeper than that. What we are now observing is the existence of irreducibly complex systems within irreducibly complex systems. How random mutations, coupled with natural selection, could have assembled such a finely set-up system is a question to which I defy any Darwinist to give a sensible answer.
    http://www.evolutionnews.org/2.....50911.html

    Biologist Howard Berg at Harvard calls the Bacterial Flagellum

    “the most efficient machine in the universe.”

    The flagellum has steadfastly resisted all attempts to elucidate its plausible origination by Darwinian processes, much less has anyone ever actually evolved a flagellum from scratch in the laboratory;

    Genetic Entropy Refutation of Nick Matzke’s TTSS (type III secretion system) to Flagellum Evolutionary Narrative:
    Excerpt: Comparative genomic analysis show that flagellar genes have been differentially lost in endosymbiotic bacteria of insects. Only proteins involved in protein export within the flagella assembly pathway (type III secretion system and the basal-body) have been kept…
    http://mbe.oxfordjournals.org/.....t/msn153v1

  39. Sequence convergence seems rather more common than was first thought, but that might simply be because we have much more gene and genome data to sift though than was previously possible.

    I would say that any homology at the sequence level could be ancestral, the product of either adaptive convergence or could be the result of homoplasious mutations. It is only by looking at these sequences in a phylogenetic context that we can begin to tease these possibilities apart. Signatures have been found in genes, and it looks like work has begun on whole genomes, to work out the frequency with which sequence convergence occurs.

    You might also be interested in the following:

    Liu, Y, Rossiter SJ, Han X, Cotton JA and Zhang S (2010) Cetaceans on a molecular fast track to ultrasonic hearing. Current Biology 20, 1834-1839.

    Davies KTJ, Cotton JA, Kirwan J, Teeling EC and /Rossiter SJ/ (2012)

    Parallel signatures of sequence evolution among hearing genes in echolocating mammals: an emerging model of genetic convergence. Heredity, DOI 10.1038/hdy.2011.119
    http://www.nature.com/hdy/jour.....1119a.html

  40. I didn’t mention the t3ss in my post, and I’m not sure how that paper refutes Nick’s hypothesis.

  41. 41

    “the authors found significant cases of molecular convergence in 13 mitochondrially-encoded proteins of lizards and snakes.”

    The key phrase here is “across 13 proteins”. They found about 100 convergent sites across 13 proteins. Which is a handful per protein, which is what I said was typical for reported cases. Proteins are typically 100-500+ amino acids. (And, those proteins are a small subset of the ~20,000 proteins in these reptile genomes.)

  42. Sorry Starbuck, my bad! completely wrong topic,,,,,, should have read more carefully before I posted.

  43. No problemo

  44. Starbucks:

    I am well aware that BLASTing these flagellar rod proteins will result in hits with each other. That’s why I said that the E-values are in fact significant with these sequences. The point really isn’t if good sequence similarity can be established for these proteins; rather, the question is if this sequence similarity is the result of gene duplication of convergent evolution at the molecular level.

  45. But I bet you don’t actually mean convergence. Convergence of significant sequence similarity like that seen within the rod would be so improbable that it would likely indicate either ancestry or special creation, and it’s the latter that you’re really advocating isn’t it? There is such a thing as adaptive convergence, but what is your evidence for that with regard to the rod? It seems to me that the only reason why you reject gene duplication as an explanation for the rod is that you want Genesis 1 to be literally true.

  46. But I bet you don’t actually mean convergence. Convergence of significant sequence similarity like that seen within the rod would be so improbable that it would likely indicate either ancestry or special creation, and it’s the latter that you’re really advocating isn’t it? There is such a thing as adaptive convergence, but what is your evidence for that with regard to the rod?

    But I do mean convergence at the molecular level, and more precisely adaptive convergence, whereby this sequence similarity is the result of similar functional constraints on the amino acid sequences of these proteins. Thus, natural selection is in the equation so it’s not all that improbable.

    There are some clues for this view, too. For starters, while the FlgK in Salmonella is closer in sequence identity to Salmonella FlgE than to Buchnera FlgE, FlgK still shares about 37 residues that are identical in Buchnera FlgE, but are not identical in Salmonella FlgE, even though, on the whole, FlgK of Salmonella is closer to Salmonella FlgE. Given that there are 74 identical positions when we align FlgK and Buchnera FlgE, this means that 50% of these positions could possibly be the result of convergent evolution. Admittedly, this could be explained away by rapid sequence divergence on the part of Salmonella FlgE, but this is just a bit ad hoc.

    I suspect that those “convergent” positions are the result of adaptive evolution, rather than simply being neutral, and this can be tested using some cool techniques.

    It seems to me that the only reason why you reject gene duplication as an explanation for the rod is that you want Genesis 1 to be literally true.

    O.O Dear me. The topic changes from biology to religion. And guess what? It’s not I who is changing the topic to religion. It might interest you to know that I’m not even claiming to be a theist – I may very well be an atheist, an agnostic, or a theist – I’m not saying. But, for the record, no, I don’t accept Genesis as true. So, please, please stop assuming things, okay?

  47. But you don’t say why those positions would be better explained by convergence, what is the signature, why isn’t copying an inferior explanation?

  48. The discussion of whether amino acid sequence similarity can be explained by convergent evolution is interesting but besides the point. Behe was quite willing to accept the Thornton group’s (non-convergent) evolutionary explanation for the different variety of V-ATPase. The question is whether this exposes a weakness in Behe’s view that the origin of irreducibly complex systems poses a significant challenge to non-intelligently guided evolution.

    I think Behe is correct in maintaining that it doesn’t expose a weakness in his view. What Thornton’s group has succeeded in doing is showing how an IC system can become more complex. It does not succeed in showing how an IC system came into existence.

    Let’s suppose that only the fungi variety of the V-ATPase existed, and Thornton’s group was able to discover that it arose from a simpler form of V-ATPase. But this simpler form is itself IC. Would they have weakened Behe’s case? Certainly not very significantly. For they still haven’t shown how the simpler IC system came to be.

    So I find Thornton group’s work to be very interesting, but not very enlightening to the ID debate.

  49. “All DNA does is code”

    That is a lot. The problem is there is no adequate naturalistic explanation of code emergence without agency. Physicality is informationally inert, on massive observation.

  50. So, nullasalus, how are you interpreting the word “degradation” in Behe’s piece? What do you think he means by it?

  51. 51

    I agree with this partially, but really, how many “irreducible” systems which turn out to actually be *reducible* does it take before we admit that there is significant reason to doubt that “all parts required in system X at time 0 years before present-day” is not any kind of argument for “all those parts were required in system X at any time throughout evolutionary history, therefore it couldn’t gradually evolve.”

    You would do better to redefine “part” so that it is meant in terms of a logically-required function, rather than a specific protein. It is apparently trivial to evolve proteins that are required, even though the ancestor with a similar function didn’t strictly need the extra proteins.

    Behe actually makes his argument this way sometimes in Darwin’s Black Box — e.g., for him, the flagellum had *three* parts — motor, rotor, stator. But soon after, everyone got impressed by the large number of “required” proteins (meaning some knockout mutation abolished function in the lab), and that’s what the debate became about.

    But if you move back to that argument, (1) no more snowing the public with “ooh, look at the high number of required parts”, and (2) no more “Hey, we did a knockout experiment, this is ID research, look at us, take us seriously when we say there is ID research!!!” (Never mind that everyone since forever has done knockout experiments, and that knocking out a part is nothing like reversing evolution to test the functionality of ancestral stages, no more that cutting off someone’s head helps you understand the evolution of heads.)

    Unfortunately, (2) is Casey Luskin’s favorite argument, in particular it’s the core of his argument about why ID was misjudged in the Dover case. So, I predict no one is going to abandon the “protein list = parts list” approach, and thus Thornton’s work will remain highly relevant.

  52. Nick: “You would do better to redefine “part” so that it is meant in terms of a logically-required function, rather than a specific protein.

    Yes, I think that would be a better approach.

    It is apparently trivial to evolve proteins that are required, even though the ancestor with a similar function didn’t strictly need the extra proteins.

    I’m not quite sure what you mean by “trivial.” In the case of V-ATPase, apparently what was needed was a specific kind of wheel. It seems logically possible that originally V-ATPase was just one very complex protein, that through a series of gene duplications became five and one, and then four, one and one. But what happened is that the first original, very complex protein became less and less complex as it was replaced by simpler and simpler proteins. I think that’s a very significant fact, which shouldn’t be overlooked. How did that original, very complex protein come into existence? The trivial part, it seems to me, is the way it evolved into more, but simpler proteins.

  53. 53

    Nick Matzke,

    Ditto for “information”…

    Reading your comments above, the ‘ditto’ part of this seems to indicate that ID proponents “rely on an arbitrary and continuously-changing definition” of information.

    I certainly agree that persons (on both sides) have various definitons of information. Perhaps this happens for various reasons, but it very often seems to lead to an anthropomorphic view of information – which is understandable, but not neccesary.

    Since we live in a material universe where information has material effects and must be transfered from material substrates, perhaps you could end the confusion and provide an unambiguous view.

    I had the opportunity to approach Larry Moran on this issue, based solely on the physicality of information transfer. Unfortunately, after giving Dr Moran an overview, he decided not to engage the conversation. Perhaps you could take a look at those observations and point to where they are arbitrary with regard to the material evidence.

    Thanks

  54. But you don’t say why those positions would be better explained by convergence, what is the signature, why isn’t copying an inferior explanation?

    Well, the hypothesis that the sequence similarity observed among FlgBCEFGK is due to convergence at the molecular level basically predicts that convergent evolution will occur among independent lineages. I.e., it would predict that, although “the FlgK in Salmonella is closer in sequence identity to Salmonella FlgE than to Buchnera FlgE, FlgK still shares about 37 residues that are identical in Buchnera FlgE, but are not identical in Salmonella FlgE, even though, on the whole, FlgK of Salmonella is closer to Salmonella FlgE.” The hypothesis of plain ole’ gene duplication doesn’t predict anything like this. On the contrary, it predicts that the bulk of the residues shared between Salmonella FlgK and Buchnera FlgE would be the result of common descent, rather than convergence. But if this was true, then we would expect these 37 identical positions shared between Salmonella FlgK and Buchnera FlgE to also be found in Salmonella FlgE. But we don’t. This can be explained away by rapid sequence divergence on the part of Salmonella FlgE, but this explanation is a bit ad hoc.

    Also, consider that when makes an extensive sequence alignment of, say, FlgB, spanning many bacteria phyla, on average only about 6 different amino acid residues are allowed for every position (excluding gaps). The positions of other flagellar rod proteins, like FlgC, are under even tighter functional constraint. Thus, convergent evolution at the molecular level wouldn’t be that implausible at all, since only little more than 25% of the amino acid repertoire can be used.

    Gene duplication explains the sequence similarity shared among these proteins, but when we start digging under the surface we start seeing clues that convergent evolution might actually be at the root of this sequence similarity.

  55. Nick, I can think of a simple chemical reaction taking more than one chemical, e.g. neutralisation which requires some acid and alkali. Can neutralisation phenomenon be reduced to just acid or just alkali?

  56. 56

    Hi BiPed,

    With regard to information, the main question I’m interested in is, if a gene is duplicated, and one copy get modified such that it has a different specificity or function, has the amount of information in the genome increased?

    I think, on any reasonable definition of “information”, the answer is “yes”. But this causes a problem for creationists/ID advocates, because they have invested a huge amount in the proposition that only intelligence can produce new information, and that natural processes such as evolution cannot.

    Thus, to defend their assertion, they have to invent all kinds of unreasonable and question-begging “definitions” of “information”.

    So, what’s your answer to the gene duplication question?

  57. 57

    The ancestral inner membrane ring of the V-ATPase wasn’t “very complex”, it was one short protein (less than 100 amino acids). The one gene is used to synthesize hundreds of copies of the protein, and they assemble into monomeric rings in the inner membrane.

    The one-gene version is still the situation in many bacteria, which have the homologous FoF1-ATPase, where the inner membrane ring protein is called the c-subunit of the Fo portion of the system. (Except for those bacteria which have duplicated the gene/protein for the c subunit, which has happened at least in chloroplasts and, I think, in other cases also.)

    Again, you’ve got a severe problem with words like “complicated” if one gene is considered more complex than several genes. Any IDist anywhere, unless they had just been beaten over the head by the Thornton lab’s work, would say that the multiprotein system is more complex, that it’s a finely-tuned irreducible machine, that all those proteins working together must have come together at once and are an insuperable obstacle to Darwinism, yadda yadda yadda. You can’t just abandon all those standard ID assertions like they were never made (especially when they will instantly be made again the next time some random system comes up.)

  58. 58

    You are making all kinds of dubious assumptions and assertions here. You need to learn something about the statistics of homology searches, the high statistical improbability of a sequence match *even* in the case of “strong” constraints on the sequence, etc. And then get it peer-reviewed and published. Literally hundreds of thousands of scientists and entire fields of research, all the genomics databases, etc., make use of homology and the statistical tools I have cited (like BLAST). It’s not just little old me making the assertion that convergence is not a likely explanation of sequence similarity.

    Also: if you want to do a serious analysis of the rod proteins: estimate a phylogeny, estimate a phylogeny, estimate a phylogeny. Random statements about X sharing certain similarities to Y don’t mean much, you need to look at the overall picture, which is a phylogeny.

  59. 59

    Nick Matzke,

    Of course, it cannot go unnoticed that you failed to engage the material evidence at any level whatsoever, not even to say that you’re disinterested in it – if that’s even possible. I am not sure how your response, one demonstrating such clear avoidance of the issue in such an obvious manner, will age for a person like yourself; a person who has been something of activist in these matters.

    I would think it will not age well.

  60. I’m not sure if I understand you exactly. Homology
    is not due to sequence similarity, but rather sequence similarity is often a result of homology if there is not too much divergence. Homology of sequence is due to common ancestry, so what the sequences do afterwards (diverge, or converge) doesn’t affect it.

    I’m not sure if I understood your point fully though, so if I have misunderstood it, please write back and I will try to answer further.

  61. Nick: Again, you’ve got a severe problem with words like “complicated” if one gene is considered more complex than several genes.

    No, I don’t think there is a problem. If one gene accomplished what it now takes several copies of a gene to accomplish, then it seems that the first gene was at least equally “complicated” as the several copies of the second gene are now. What (non-intelligently guided) theories of evolution need to demonstrate is the ability of genes to gain function, not lose function, which all that Thornton’s group has demonstrated.

  62. You realize, of course, that Behe’s review article lists at least three instances of gain of function.

  63. And do you realize that those supposed ‘gain of functions’ in Behe’s paper, were preceded by deletion events, or was that little fact just a ‘inconvenient truth’ you forgot to mention in your attempt to decieve?

    4 nucleotide deletion in lysis gene
    of MS2
    Reading frame restored by deletions,
    insertions
    G,G Licis and van Duin
    (2006)

    Viruses manipulated to be defective
    Deletion of 19 intercistronic
    nucleotides from RNA virus MS2
    containing Shine-Dalgarno
    sequence and two hairpins
    One revertant deleted 6 nucleotides;
    another duplicated an adjoining 14-
    nucleotide sequence; missing
    functional coded elements
    substantially restored
    G,G Olsthoorn and van
    Duin (1996)

    Viruses forced to be interdependent
    Separate viruses, f1 and IKe,
    engineered to carry distinct
    antibiotic resistance markers
    In media containing both antibiotics,
    phages co-packaged into f1 protein
    coats; two-thirds of IKe genome
    deleted, second antibiotic gene
    captured by f1
    L,M
    G
    Sachs and Bull (2005)
    http://www.lehigh.edu/~inbios/....._paper.pdf

    Moreover, far from you proving that these trivial ‘return of function’, (which is far more appropriate than ‘gain of function’), mutations were random, the ‘mutations are in fact just more stunning proof of the sophisticated programming in the cell that calculated a appropriate response to a artificially induced environmental stress.

  64. should read:

    appropriate response to a artificially induced defect.

  65. Behe excluded any studies that included more powerful gain of function possibilities, such as duplication events or horizontal gene transfer.

    If you limit your study to short term point mutation experiments, you will get point mutation results.

  66. And your problem still remains that you were deliberately misleading to begin with, and are still deliberately misleading with duplication events or horizontal gene transfer since these events are ‘non-random’ number one, and number two they clearly do not address the elephant in the living room problem of the generation of functional sequence complexity, not to mention they do not address the higher levels of information above functional sequence complexity that are completely ignored in the reductive materialistic framework of neo_Darwinism:

    notes:

    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)

    Epigenetics and the “Piano” Metaphor – January 2012
    Excerpt: And this is only the construction of proteins we’re talking about. It leaves out of the picture entirely the higher-level components — tissues, organs, the whole body plan that draws all the lower-level stuff together into a coherent, functioning form. What we should really be talking about is not a lone piano but a vast orchestra under the directing guidance of an unknown conductor fulfilling an artistic vision, organizing and transcending the music of the assembly of individual players.
    http://www.evolutionnews.org/2.....54731.html

    Revisiting the Central Dogma in the 21st Century – James A. Shapiro – 2009
    Excerpt (Page 12): Underlying the central dogma and conventional views of genome evolution was the idea that the genome is a stable structure that changes rarely and accidentally by chemical fluctuations (106) or replication errors. This view has had to change with the realization that maintenance of genome stability is an active cellular function and the discovery of numerous dedicated biochemical systems for restructuring DNA molecules.(107–110) Genetic change is almost always the result of cellular action on the genome. These natural processes are analogous to human genetic engineering,,, (Page 14) Genome change arises as a consequence of natural genetic engineering, not from accidents. Replication errors and DNA damage are subject to cell surveillance and correction. When DNA damage correction does produce novel genetic structures, natural genetic engineering functions, such as mutator polymerases and nonhomologous end-joining complexes, are involved. Realizing that DNA change is a biochemical process means that it is subject to regulation like other cellular activities. Thus, we expect to see genome change occurring in response to different stimuli (Table 1) and operating nonrandomly throughout the genome, guided by various types of intermolecular contacts (Table 1 of Ref. 112).
    http://shapiro.bsd.uchicago.ed.....0Dogma.pdf

    Modern Synthesis of Neo-Darwinism (Genetic Reductionism) Is Dead – Paul Nelson – video
    http://www.metacafe.com/watch/5548184/

    Falsification Of Neo-Darwinism by Quantum Entanglement/Information
    https://docs.google.com/document/d/1p8AQgqFqiRQwyaF8t1_CKTPQ9duN8FHU9-pV4oBDOVs/edit?hl=en_US

  67. moreover perhaps you would care to list the studies that Dr. Behe so carelessly overlooked so that we can, once and for all, see the almighty power of your beloved theory of evolution do anything whatsoever besides break things:

    “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/

  68. 68

    Wow. Way to totally not answer one very simple, not-hard, not-trick question.

  69. I too am interested in hearing Upright Biped’s answer to that question. How about it, Upright?

  70. 70

    Nick, are you referring to where I asked you substantiate your comments upthread by taking a quick look at a page, and you returned to say absolutely nothing whatsoever about the content. Are you referring to where you immediately changed the subject?

    If that was indeed what you meant, then I agree with you – “wow”.

  71. 71

    Champignon,

    If Nick Matzke had a substantive refutation of the observations made, he would have voiced it.

    I have no particular desire to entertain a conversation otherwise.

  72. Upright,

    He’s referring to this question, as you well know:

    if a gene is duplicated, and one copy get modified such that it has a different specificity or function, has the amount of information in the genome increased?

    What is your answer?

  73. I like your staying on target, UB.

    I have a question of my own about the question.

    if a gene is duplicated, and one copy get modified such that it has a different specificity or function, has the amount of information in the genome increased?

    If I take a bicycle, then crush it such that the resulting lump of metal/plastic could be used as a doorstop, would this be an example of the bicycle being ‘modified such that it has a different specificity or function’? If so, should this be regarded as an increase in information?

  74. Homology of sequence is due to common ancestry, so what the sequences do afterwards (diverge, or converge) doesn’t affect it.

    Quite true, but if the sequence similarity shared among these flagellar rod proteins are the result of gene duplication (i.e., common ancestry), we wouldn’t predict that fully half of the residues shared between Salmonella FlgK and Buchnera FlgE are not shared between Salmonella FlgK and Salmonella FlgE. But this fits neatly within the hypothesis that convergent evolution has played a major role in generating the sequence similarity shared among these rod proteins. We would expect stuff like that if this sequence similarity is indeed the result of convergent evolution, but this isn’t expected if this sequence similarity is essentially the result of common ancestry.

  75. You are making all kinds of dubious assumptions and assertions here. You need to learn something about the statistics of homology searches, the high statistical improbability of a sequence match *even* in the case of “strong” constraints on the sequence, etc. And then get it peer-reviewed and published. Literally hundreds of thousands of scientists and entire fields of research, all the genomics databases, etc., make use of homology and the statistical tools I have cited (like BLAST). It’s not just little old me making the assertion that convergence is not a likely explanation of sequence similarity.

    Indeed? What kind of dubious assertions and assumptions am I making? If only ~25% of the amino acid repertoire can be used among the flagellar rod proteins, then ~20% sequence identity is expected from chance alone. Couple this with the fact that we’ve also got natural selection in the equation, and convergence at the molecular level becomes a bit plausible. You seem to be under the impression that I am repudiating BLAST et al., but I am not. E.g., E-values don’t take into account the role of natural selection; they indicate if a hit is significant, not if a hit is the result of common ancestry.

  76. 76

    Indeed? What kind of dubious assertions and assumptions am I making? If only ~25% of the amino acid repertoire can be used among the flagellar rod proteins, then ~20% sequence identity is expected from chance alone. Couple this with the fact that we’ve also got natural selection in the equation, and convergence at the molecular level becomes a bit plausible. You seem to be under the impression that I am repudiating BLAST et al., but I am not. E.g., E-values don’t take into account the role of natural selection; they indicate if a hit is significant, not if a hit is the result of common ancestry.

    A few points:

    1. Nothing is ever as simple as “only 25% of the amino acids” can be used at a site. Rather, different amino acids occur at different frequencies. These frequencies are what go into the calculation of scores like e-values, or likelihoods of sequence data under different phylogenies and substitution models. Thus to judge the relative probability of different explanations of the observed sequence data, you really really really need to do it in an explicitly statistical way, not just eyeball it and cherry pick some bit of the data you think supports your position.

    2. The variation you observe in a particular site in whatever collection of axial proteins you are looking at is likely

    less than the variation you would observe if you observed all available homologous sequences in the databases, which is very likely

    less than the variation you would observe if you could observe all currently-living variants of the sequence, which is very very likely

    less than the variation you would observe if you could observe all variants of the sequence that existed at any time in history, which is certainly

    much much less than the variation you would observe if you counted all of the possible ways of building axial filament structures with the 20 amino acids, given what we know about the fact that entirely different amino acid sequences can produce basically identical functions, binding sites, etc., plus we know that entirely dissimilar, nonhomologous proteins *are* observed to produce axial filaments (in archaeal flagella) and in numerous other pilus structures.

    Your observed limitation on amino acid variation, even if you could be sure it accurately described the True Complete limits on amino acid variation in the early stages I described above, wouldn’t help at all with the later stages.

    3. And it doesn’t matter anyway, because even if the most extreme statement is taken as true, and, say, 20% amino acid similarity at particular sites is expected at random due to limitations in allowed amino acid positions (this is already a huge amount of convergence), well then, you multiply by 10 or 20 or 30 sites and your chance of independently getting detailed similarity across the alignment (which is what BLAST looks at) converges to 0 very quickly. DNA, after all, has only 4 allowed sites, and “random” similarity is therefore something like 25% (depending on G+C content), and yet BLAST and homology searches work perfectly fine anyway.

    4. You could, if you wanted, build a statistical model wherein you asserted that the limited variation you observe at each site really is all the variation that could ever be tolerated at each site (a “high-convergence” model). Then you could compare the chances of getting the observed similarity independently, vs. the chance of getting it through copying up the inferred phylogenetic tree. A standard statistic like AIC could be used to make the judgment. If you can statistically significantly beat the copying-up-the-phylogenetic-tree model, well then, go ahead and publish. But without that kind of evidence, you won’t get anywhere at all with anyone who knows bioinformatics. This is science, after all, and Genbank and NCBI and BLAST and the rest weren’t built by a few schmucks who thought this stuff up yesterday, these methods have been pretty extensively tested in thousands of publications.

    Re: this:

    On the contrary, it predicts that the bulk of the residues shared between Salmonella FlgK and Buchnera FlgE would be the result of common descent, rather than convergence. But if this was true, then we would expect these 37 identical positions shared between Salmonella FlgK and Buchnera FlgE to also be found in Salmonella FlgE. But we don’t. This can be explained away by rapid sequence divergence on the part of Salmonella FlgE, but this explanation is a bit ad hoc.

    I would need to take a detailed look at the sequences, alignment length, phylogeny, related sequences, etc., to get a sense of whether or not this is really surprising. But, one thing to watch out for is that with the huge mass of sequencing data going into the databases these days, sequences are often mis-named, either through algorithm or human error.

    Another thing to watch out for is selective sampling of the best BLAST hit. If one BLASTS protein A, the database will return a bunch of homologous copies of A, and then start returning sequences from protein B, the sister group. However, out of say 1000 available B sequences, a few of them will be much closer to A than the average B sequence, because percentage similarity between sister groups will fall into a bell curve, and some sequence *has* to be on the end of the bell curve closer to A.

    Again (and I will say it again and again) the way to sort such things out is with a phylogeny of all the sequences, or a fair sample of the sequences. Even if massive convergence actually happened in real life, you would probably need to calculate a phylogeny (and then observe massive weirdness) in order to be sure you were seeing it.

  77. 77

    BiPed,

    I read through your very long essay, and saw neither (a) an actual concise definition of information, nor (b) one that would answer my very simple, obvious, basic, simple question, so I asked my question. I do so again.

  78. If I take a bicycle, then crush it such that the resulting lump of metal/plastic could be used as a doorstop, would this be an example of the bicycle being ‘modified such that it has a different specificity or function’? If so, should this be regarded as an increase in information?

    If you copy the bicycle first, so that you end up with a bicycle plus a doorstop, then yes. A little bit more.

    What if you copy a program that plots a bell curve, and the copy has a single change in a number that makes it plot a different curve? Less information or more?

    Of course, with genes, evolution is doing nothing so crude as crushing the sequences into a ball. Most/all of the sequence is retained in each duplicate. This has led, for example, to dozens and dozens of copies of MHC genes (the more genes, the more pathogens you can recognize), smell receptors, the red, green, and blue cone receptor genes in the human eye, etc. Wouldn’t these be increases in information? (Maybe you think the IDer made all those copies, I don’t care, for now I just want people to admit that such things would represent increases in information.)

  79. If you copy the bicycle first, so that you end up with a bicycle plus a doorstop, then yes. A little bit more.

    Alright, – so, take a copy, crush it into a doorstop. That’s an information gain according to you. That’s the standard you’re going for here.

    So, a followup question: would a copy of a bicycle that gets crushed into a doorstop be an example of degradation?

  80. If you copy the bicycle first, so that you end up with a bicycle plus a doorstop, then yes. A little bit more.

    Alright, – so, take a copy, crush it into a doorstop. That’s an information gain according to you. That’s the standard you’re going for here.

    So, a followup question: would a copy of a bicycle that gets crushed into a doorstop be an example of degradation?

  81. Onlookers, note the entertaining dynamic at work here. Upright Biped squirms for a while at the sight of Nick’s question, then goes into hiding.

    This is especially amusing given the way UB was lecturing Elizabeth Liddle a few hours ago:

    Do you not have any conscience at all? Are you capable of any truly genuine sense whatsoever of right and wrong in your actions regarding this matter? I don’t see it, Dr Liddle. Where is it? Are you a scientist or not?

    Allow me to show you how this is done Dr Liddle:

    “Yes, design proponents have produced some interesting evidence with regard to the rise of recorded information transfer in biological systems. I personally remain unconvinced by that evidence, but I cannot in good conscience maintain that the evidence does not exist or that it cannot be legitimately considered as evidence of design”.

    Now tell me, why is such a modest yet materially-honest response so far beyond your personal and professional capabilities Dr Liddle?

    LOL. Okay, Upright, here’s how it’s done: “Yes, Nick, gene duplication followed by modification of the copy can result in an increase in information.”

    Now tell me, Upright, why is such a modest yet materially honest response so far beyond your personal and professional capabilities?

    Meanwhile, nullasalus tiptoes around Nick’s question, trying to figure out how he can spin “information gain” into “degradation”.

    Stay tuned, onlookers. This should be good.

  82. Meanwhile, nullasalus tiptoes around Nick’s question, trying to figure out how he can spin “information gain” into “degradation”.

    Ladies and gentlemen, boys and girls – step right up and watch Champ try to run amateur defense for the one and only Nick Matzke!

    Gaze in amazement as Champ tries to claim that a bicycle being smashed into a lump capable of being used as a doorstop is not an example of degradation!

    Gasp with astonishment as Champ fails to grasp why defining the smashing of a bicycle into a heavy lump as “information gain” may impact discussions of Thornton’s lab work in ways neither he nor Matzke will appreciate!

    Look on in wonderment as Champ attributes ID beliefs to the man who regards ID as not science! Be baffled at his ability to react to polite questioning of his hero’s logic with hostility!

    Can we expect blustering? Can we expect flustering? Yes, folks, all this and more – everything except accepting the obvious: that smashing a bicycle into a compact, heavy lump is an example of degradation! He regards this as “spin”, members of this viewing audience (all 5 of you). Get the popcorn, put on your 3D glasses, and enjoy the show!

    Those of you in the front row, please have your body-sized plastic sheet ready. What Champ spews is a sight to behold, but you don’t want to have to wash this out of your clothes if it splashes onto you. ;)

  83. nullasalus; 8)

  84. hey nick

    what about ‘minimal complexity”?

    a 100 aa protein is still very complex protein and have a very large sequence space(20^100). so its not so simple at all.

    if you want to design a new ptoein that bind 2 substrate, you need a minimum 2 binding site. a simple binding site need somthing like 50 aa(from the paper of szostak in 2004)

  85. if a gene is duplicated, and one copy get modified such that it has a different specificity or function, has the amount of information in the genome increased?

    1- In a design scenario, no

    2- In a non-design scenario you are question-begging

  86. Here is an experiment evos will not conduct-

    Take those proteins Throton et all were studying, put them in a flask and see if they will self-assemble into V-ATPase.

    Or take all of the flagella proteins and do the same.

    If nothing happens then self-assembly would be shot-down…

  87. mk- forgetaboutit- Nick needs to start with what needs explaining in the first place. Gene duplications as a mechanism of Darwinian evolution was shot-down by Dr Spetenr in “Not By Chance”- Nick sed he has read the book yet cannot rememebr any of it.

    LoL!

  88. Nick M

    With regard to information, the main question I’m interested in is, if a gene is duplicated, and one copy get modified such that it has a different specificity or function, has the amount of information in the genome increased?

    1- In a design scenario, no

    2- In a non-design scenario you are question-begging

    I think, on any reasonable definition of “information”, the answer is “yes”. But this causes a problem for creationists/ID advocates, because they have invested a huge amount in the proposition that only intelligence can produce new information, and that natural processes such as evolution cannot.

    Reference please- I know you are making that up, Nick.

  89. I think, on any reasonable definition of “information”, the answer is “yes”. But this causes a problem for creationists/ID advocates, because they have invested a huge amount in the proposition that only intelligence can produce new information, and that natural processes such as evolution cannot.

    Reference please- I know you are making that up, Nick.

    Not sure which of Nick’s two sentences you’re referring to. If it’s the second, here are a few references.

    Dembski and Marks, Life’s Conservation Law:

    The challenge of intelligent design, and of this paper in particular, is to show that when natural systems exhibit intelligence by producing information, they have in fact not created it from scratch but merely shuffled around existing information. Nature is a matrix for expressing already existent information. But the ultimate source of that information resides in an intelligence not reducible to nature.

    Stephen Meyer, Signature in the Cell:

    So should we think of information as thought — as a kind of mental chimera etched in stone or burned onto compact discs? Or can we define information less abstractly as, perhaps, just an improbable arrangement of matter?

    Whatever information is — whether thought or an elaborate arrangement of matter — one thing seems clear. What humans recognize as information certainly originates from conscious or intelligent activity.

    (Emphasis in original.)

  90. Hi R0bb,

    1- Design is a natural process

    2- ID is not anti-evolution

    3- Nick’s “example” is using already existing information that needs to be explained in the first place

    4- The argument is that stochastic processes can create CSI from scratch- meaning where there wasn’t any SI in the first place.

  91. 91

    I notice that Nick responded overnight. I will be out most of the afternoon, but will be most happy to return and respond later today or evening.

  92. Let’s say a bicycle has 1 million bits of information and a crushed bicycle lump has 1 bit. *If you copy the bicycle first*, then bicycle + lump has more information than bicycle plus nothing, doesn’t it?

    And, like I noted, gene duplication and modification is nothing nearly so crude.

    The fact that you can’t just say “yes” to the statement that duplication + divergence is an increase in information, is exaclty the problem with the ID definition of “information” that I am getting at here.

  93. So I guess Meyer’s “Law of Conservation of Information”, isn’t, then.

  94. Joe,
    Interesting ideas.

    Nick’s “example” is using already existing information that needs to be explained in the first place

    If Nick cannot use the example for the reason you have pointed out then presumably you have an alternative explanation in place that you can supply?

    Otherwise it seems to me that you are in the same boat as Nick – no better or no worse, except that Nick can explain may things after the subsequent arrival of the information in question, and you cannot.

  95. Does learning constitute shuffling information around? The process of variation and selection transfers information from the environment to the genome, at least the genome viewed from the perspective of the population.

    That could be characterized as work, which violates no conservation laws, regardless of how finely defined.

  96. Learning, at its simplest, involves repeating responses that give good results and inhibiting responses that give none, or bad.

    It’s built into the Darwinian algorithm, and also into Hebb’s rule, also called “neural Darwinism”.

    I don’t think it violates any conservation laws. In fact, I think you could argue that it follows them:

    http://www.ncbi.nlm.nih.gov/pm.....MC2660582/

  97. Peter Griffin:

    If Nick cannot use the example for the reason you have pointed out then presumably you have an alternative explanation in place that you can supply?

    Alternattive explanation for what?

    Otherwise it seems to me that you are in the same boat as Nick – no better or no worse, except that Nick can explain may things after the subsequent arrival of the information in question, and you cannot.

    1- Nick’s “explanations” lack evidentiary support

    2- ID is not anti-evolution

    3- Think targeted searches

  98. Nick:

    So I guess Meyer’s “Law of Conservation of Information”, isn’t, then.

    No Nick- you just don’t know what you are talking about, as usual.

  99. Nick:

    The fact that you can’t just say “yes” to the statement that duplication + divergence is an increase in information, is exaclty the problem with the ID definition of “information” that I am getting at here.

    Actually the “problem” is you and your misunderstanding.

  100. I’m just suggesting that shuffling information around is not a limitation in a feedback driven system.

    The concept of work in physics allows entropy to be selective shuffled from one system to another. Much as evaporation and rain allow the river to flow uphill.

    Metabolism, reproduction, fecundity and selection provide the means for information to flow from the environment to the genome. Regardless of how you define entropy or whether you posit a law of conservation, evolution does not violate any conservation law.

  101. 101

    Joe,

    No Nick- you just don’t know what you are talking about, as usual.

    Point and match to Nick I’d say. If you are unable to actually address his points then why even bother adding a comment? It only draws attention to your inability to respond in a cogent manner.

  102. Yes, indeed :)

    That paper’s quite interesting, btw.

  103. I would approach this case by trying to rule out reasonable alternative hypothesis. First, it is quite common in situations such as the case you cite, that differing levels of divergence following gene duplication and/or speciation can explain the degree of similarity. For example, if FigK has relatively fast evolution in Salmonella, but F1gE has relatively fast evolution in Buchnera, then Buchnera F1gK and Salmonella F1gE would be closest. Try drawing it out if it is not clear.

    Secondarily, I would always check that the convergence might be explainable by chance and neutral drift. All of this requires more detailed analysis.

  104. 104

    Alternattive explanation for what?

    Well, anything at all really. Take your pick.

    Just tell me what ID does explain, not what Darwinism does not.

    - Nick’s “explanations” lack evidentiary support

    And the evidence for your position is what exactly? How and where did “the information” arrive?

    3- Think targeted searches

    When is the target set?
    When is the target search activated?
    Where is the target information held?
    How is it preserved?
    When is it introduced?
    How can you tell if it still exists at all?

  105. 105

    Joe.

    You seem to hold great stock in “targeted searches”.

    Well answer me a question then.

    If the search is targeted then the target was set in advance.

    So if that’s the case then why “search” at all? Why not just put in the required information directly, if it’s to hand? Why edit DNA at all (or how do you claim it is done?) to introduce the target when you can, well, just introduce the actual required data there and then?

    And when do you claim these targets were set? Billions of years ago? Yesterday?

    And if the targets are set in advance that means that the target setter knows the future! So you believe in an alien that can tell the future?

    Joe, you are trolling with me, a newbie, are you not!

    I can always tell!

  106. 106

    Joe,
    Who is making that claim? That such systems arose from being brought into the same location and randomly shuffled?

    Can you provide “evidentiary support” for your claims, you were just saying that Nick could not and used that exact phrase. The question is (as no ID supporter seems willing to call you on it) can you support even a single one of your claims when asked?

    Can you? Citation please.

    It’s only you that claim that flagella arose in a single step, design. Nobody else.

  107. Peter:

    You seem to hold great stock in “targeted searches”.

    For a good reason-> they have been demonstrated to work.

    If the search is targeted then the target was set in advance.

    In some manner, yes.

    Ya see when engineers were looking for an antenna to do a spcific job they didn’t know what teh antenna would look like, but they knew what it had to do. So they used a targeted search to get the antenna required based on the specification provided.

    I don’t know when the targets were set. If I had all the answers then I wouldn’t need science and if your position had any positive evidence then you wouldn’t care about ID.

  108. Peter,

    One clueless evo trying to support another clueless evo does not amount to evidence of any kind.

    That said I have already responded to Nick, many times. I am sick of his willful ignorance.

  109. Peter:

    Who is making that claim?

    What claim?

    That such systems arose from being brought into the same location and randomly shuffled?

    Huh? I am just asking for evidence tat stochastic processes can contruct the protein configuration Nick is talking about.

    It’s only you that claim that flagella arose in a single step, design.

    Except design doesn’t require just a single step. And if there was any evidence that any flagellum could arise via stochastic processes we wouldn’t be having this discussion.

  110. 110

    Got any examples from biology?

  111. 111

    Joe,

    don’t know when the targets were set.

    If you don’t know a single thing about them apart from they seem to help, in some way, your argument, then how do you know they actually exist?

    After all, if you can’t tell me anything at all about them apart from “they are useful to reach targets” how can you claim they even exist in biological organisms, never mind that they support ID in some way?

  112. 112

    Joe,

    I am just asking for evidence tat stochastic processes can contruct the protein configuration Nick is talking about.

    Type “protein evolution” into google scholar.

    Except design doesn’t require just a single step.

    Then design a protein that performs the same function as Lactase but 10 times more efficiently.

    You can’t. Nobody can. Only evolution could.

    And if there was any evidence that any flagellum could arise via stochastic processes we wouldn’t be having this discussion.

    There is such evidence for many of the proteins, your gap shrinks every day.

    And which specific flagellum do you mean?

  113. 113

    Joe,

    Ya see when engineers were looking for an antenna to do a spcific job they didn’t know what teh antenna would look like, but they knew what it had to do. So they used a targeted search to get the antenna required based on the specification provided.

    So “have more progeny” could be a specification? One that the environment provides input into?

    Interesting.

  114. 114

    Joe,

    Take those proteins Throton et all were studying, put them in a flask and see if they will self-assemble into V-ATPase.

    Or take all of the flagella proteins and do the same.

    If nothing happens then self-assembly would be shot-down…

    Please provide a citation to a biologist who makes this “self-assembly from parts” claim or admit its a strawman.

  115. 115

    Nick Matzke,

    BiPed,

    I read through your very long essay, and saw neither (a) an actual concise definition of information, nor (b) one that would answer my very simple, obvious, basic, simple question, so I asked my question. I do so again.

    Well Nick, after three very clear opportunities, you have made it most obvious that you do not intend on addressing the argument being presented to you. Consequently, I feel no obligation to answer the talking point you’ve superimposed upon the conversation as a means to avoid that very argument. This lack of obligation on my part is made even more pronounced, given that the argument being presented to you makes your question non-substantive – which is why I am allowing it to qualify your question. (Feel free to challenge this characterization as a means to further ignore the evidence being presented).

    Of course, your hesitation is not only obvious, but entirely understandable as well. You simply cannot enter the argument in earnest, because you will lose. It would be no different than me entering into a debate to challenge whether the Earth is rounded. The moment you state what must be stated in order to challenge the conclusion; you would be met with questions and evidence that simply cannot be overcome. This is indicative of nothing more than being on the wrong side of the evidence.

    But since you have set your feet in clay, allow me to offer you something else to mull over. The observed physical entailments of information transfer require two material objects with specific dynamic properties. Those two objects must be coordinated, but cannot interact, and one is useless without the other. In other words, translation during protein synthesis is IC. (Feel free to challenge this characterization as a means to further ignore the evidence being presented).

  116. Upright,

    Your evasion of Nick’s simple question is very telling.

  117. What else is there Peter? What guiding/ assembling force does stochastic processes provide?

    Please be specific.

  118. Having more progeny doesn’t construct new useful protein machinery, duh.

  119. Peter, Your position doesn’t seem to know anything at all. Not a single thing.

    And I don’t have to know when the targets were set in order to know the efectoness of a targeted search.

  120. 120

    Please provide a citation to a biologist who makes this “self-assembly from parts” claim or admit its a strawman.

  121. Do you? Do you have any examples in which stocahistic processes constructed new, useful multiprotein configurations? Anything at all?

  122. As far as I know they all do- what else is there? If you cannot answer then bug off.

  123. There isn’t anything in google scholar to support the claim that V ATPase “evolved” via accumulations of random mutations. Stop bluffing.

    Then design a protein that performs the same function as Lactase but 10 times more efficiently.

    You can’t. Nobody can. Only evolution could.

    ID is not anti-evolution you equivocating coward. And there isn’t any data that stochastic processes can do it.


    And if there was any evidence that any flagellum could arise via stochastic processes we wouldn’t be having this discussion.

    There is such evidence for many of the proteins, your gap shrinks every day.

    Wishful thinking.

    And which specific flagellum do you mean?

    Your position cannot account for any of them…

  124. 124

    Joe,
    So as you cannot provide a cite then the assumption is that you are incorrect in your claims.

    If we look at the abstract of “Macromolecular organization of ATP synthase and complex I in whole mitochondria”

    We read this:

    We used electron cryotomography to study the molecular arrangement of large respiratory chain complexes in mitochondria from bovine heart, potato, and three types of fungi. Long rows of ATP synthase dimers were observed in intact mitochondria and cristae membrane fragments of all species that were examined. The dimer rows were found exclusively on tightly curved cristae edges. The distance between dimers along the rows varied, but within the dimer the distance between F1 heads was constant. The angle between monomers in the dimer was 70° or above. Complex I appeared as L-shaped densities in tomograms of reconstituted proteoliposomes. Similar densities were observed in flat membrane regions of mitochondrial membranes from all species except Saccharomyces cerevisiae and identified as complex I by quantum-dot labeling. The arrangement of respiratory chain proton pumps on flat cristae membranes and ATP synthase dimer rows along cristae edges was conserved in all species investigated. We propose that the supramolecular organization of respiratory chain complexes as proton sources and ATP synthase rows as proton sinks in the mitochondrial cristae ensures optimal conditions for efficient ATP synthesis.

    Why does that support design?

    Please provide a quotation that supports your claim that the authors believe the system was designed.

  125. Peter, Seeing that you cannot provide any citation for anything you are a waste of time.

    And how does what you quoted support design?

    1- There isn’t any evidence that stochastic processes can do it

    2- It meets the design criteria.

    And I don’t care what the authors think. If they can they can try to support the position that stochastic processes didit. But they won’t because they can’t

  126. 126

    Joe,

    There isn’t anything in google scholar to support the claim that V ATPase “evolved” via accumulations of random mutations. Stop bluffing.

    Nothing you could understand, no.

    Yet you are unable to provide a quote indicating that the authors of the papers you reference re: ATP share your belief.

    ID is not anti-evolution you equivocating coward. And there isn’t any data that stochastic processes can do it.

    So how did it happen? What detail can you provide?

    And if there was any evidence that any flagellum could arise via stochastic processes we wouldn’t be having this discussion.

    Nobody is making that claim, and that’s why there is no evidence for it.

    Your position cannot account for any of them…

    Why did the designer make so many types of flagellum Joe? Oh, that’s right, ID does not answer that sort of question.

    In that case, how does ID explain the flagellum Joe?

    “It was designed” seems to be all you’ve got, lol.

  127. Well saying it was deigned is a start Peter. and guess what? That is how it starts in archaeology and forensic science too.


    And if there was any evidence that any flagellum could arise via stochastic processes we wouldn’t be having this discussion.

    Nobody is making that claim, and that’s why there is no evidence for it.

    The theory of evolution makes that claim. Are you really that dense?

  128. 128

    Joe,

    Well saying it was deigned is a start Peter. and guess what? That is how it starts in archaeology and forensic science too.

    It’s not a start, it’s called assuming your conclusion.

    The theory of evolution makes that claim. Are you really that dense?

    Citation please. Prove it!

  129. Peter,

    Determining design is a start. Then you go from there with your invesitagtion.

    And the theory of evolution posits a mechanism of accumulations of random mutations- citation Mayr “What Evolution Is”

  130. 130

    Joe,

    Determining design is a start. Then you go from there with your invesitagtion.

    But if investigating the designer is off limits, what exactly are you investigating? Where do you go to once you’ve determined design?

    And the theory of evolution posits a mechanism of accumulations of random mutations- citation Mayr “What Evolution Is”

    Quotation please. Or retract your straw-man before I set it afire!

  131. What guiding/ assembling force does stochastic processes provide?

    The guiding force is the probability of breeding successfully in the current environment.

    It’s a stochastic process though. Stochastic processes can have non-flat probability distributions. In fact, they usually do.

  132. The guiding force is the probability of breeding successfully in the current environment.

    Which doesn’t lead to much of anything.

  133. We would be investigating the DESIGN Peter. That is why it is called Intelligent DESIGN, Peter.

    We do that so we can understand it, maybe duplicate it or reverse engineer it, fix it, maintain it, and understand its purpose.

    And I have provided enough references to support my claim of accumulations of random mutations. Obvioulsy you choked on them because you cannot grasp the simple concept of “all inclusive”.

  134. 134

    Joe,

    Which doesn’t lead to much of anything.

    That’s right Joe. I mean, what possible difference could it make in the long term if a given trait allows successful breeding in a given environment?

    Not much of anything, right?

    I mean, it’s laughable to think that it might have an effect on the information in the genome.

    It’s laughable to think that “whatever survives survives” could matter at all when talking about evolution.

    The fact is you are only able to dismiss evolution because you simply don’t understand it.

    How do I know that? Your own words?

    the probability of breeding successfully in the current environment doesn’t lead to much of anything

    Yeah, just like the probability of having longer legs won’t affect the probability of escaping the lion.

    Your fundamental willful misunderstanding of evolution reflects very badly on those here trying their best to support ID.

    I’m surprised they let you get away with it.

  135. 135

    Joe,

    We would be investigating the DESIGN Peter. That is why it is called Intelligent DESIGN, Peter.

    And what have you discovered so far from studying the design of ATP?

    So far I understand that you’ve discovered it’s designed.

    Anything else?

    We do that so we can understand it, maybe duplicate it or reverse engineer it, fix it, maintain it, and understand its purpose.

    And what have you discovered so far? Any purpose there in the genome? What is the purpose of HIV?

    And I have provided enough references to support my claim of accumulations of random mutations. Obvioulsy you choked on them because you cannot grasp the simple concept of “all inclusive”.

    And it seems you cannot grasp the concept of “selection matters” and that there are more engines of variation then random mutations.

    And you have in no way supported your claim that the only evolutionary mechanism elucidated so far are all based upon random mutations.

    SOURCES OF HERITABLE VARIATION BETWEEN INDIVIDUALS IN POPULATIONS

    Gene Structure (in DNA)

    1) point mutations

    2) deletion and insertion (“frame shift” / “indel”) mutations

    3) inversion and translocation mutations

    Gene Expression in Prokaryotes

    4) changes in promoter or terminator sequences (increasing or decreasing binding)

    5) changes in repressor binding (in prokaryotes); increasing or decreasing binding to operator sites

    6) changes in repressor binding (in prokaryotes); increasing or decreasing binding to inducers

    7) changes in repressor binding (in prokaryotes); increasing or decreasing binding to corepressors

    Gene Expression in Eukaryotes

    8) changes in activation factor function in eukaryotes (increasing or decreasing binding to promoters)

    9) changes in intron length, location, and/or editing by changes in specificity of SNRPs

    10) changes in interference/antisense RNA regulation (increasing or decreasing binding to sense RNAs)

    Gene Interactions

    11) changes in substrates or products of biochemical pathways

    12) addition or removal of gene products (especially enzymes) from biochemical pathways

    13) splitting or combining of biochemical pathways

    14) addition or alteration of pleiotropic effects, especially in response to changes in other genes/traits

    Eukaryotic Chromosome Structure

    15) gene duplication within chromosomes

    16) gene duplication in multiple chromosomes

    17) inversions involving one or more genes in one chromosome

    18) translocations involving one or more genes between two or more chromosomes

    19) deletion/insertion of one or more genes via transposons

    20) fusion of two or more chromosomes or chromosome fragments

    21) fission of one chromosome into two or more fragments

    22) changes in chromosome number via nondisjunction (aneuploidy)

    23) changes in chromosome number via autopolyploidy (especially in plants)

    24) changes in chromosome number via allopolyploidy (especially in plants)

    Eukaryotic Chromosome Function

    25) changes in regulation of multiple genes in a chromosome as a result of the foregoing structural changes

    26) changes in gene expression as result of DNA methylation

    27) changes in gene expression as result of changes in DNA-histone binding

    Genetic Recombination

    28) the exchange of non-identical genetic material between two or more individuals (i.e. sex)

    29) lateral gene transfer via plasmids and episomes (especially in prokaryotes)

    30) crossing-over (reciprocal and non-reciprocal) between sister chromatids in meiosis

    31) crossing-over (non-reciprocal) between sister chromatids in mitosis

    32) Mendelian independent assortment during meiosis

    33) hybridization

    Genome Structure and Function

    34) genome reorganization and/or reintegration

    35) partial or complete genome duplication

    36) partial or complete genome fusion

    Development (among multicellular eukaryotes, especially animals)

    37) changes in tempo and timing of gene regulation, especially in eukaryotes

    38) changes in homeotic gene regulation in eukaryotes

    39) genetic imprinting, especially via hormone-mediated DNA methylation

    Symbiosis

    40) partial or complete endosymbiosis

    41) partial or complete incorporation of unrelated organisms as part of developmental pathways (especially larval forms)

    42) changes in presence or absence of mutualists, commensals, and/or parasites

    Behavior/Neurobiology

    43) changes in behavioral anatomy, histology, and/or physiology in response to changes in biotic community

    44) changes in behavioral anatomy, histology, and/or physiology in response to changes in abiotic environment

    45) learning (including effects of use and disuse)

    Physiological Ecology

    46) changes in anatomy, histology, and/or physiology in response to changes in biotic community

    47) changes in anatomy, histology, and/or physiology in response to changes in abiotic environment

    As Allen says:

    So, next time you hear or read a creationist or IDer cite “RM & NS” as the sole explanation for evolutionary change, point out to them and everyone else that there are at least 47 different sources of variation (including “random mutations”), and at least three different processes that result from them: natural selection, sexual selection, and random genetic drift.

    http://evolutionlist.blogspot......0variation

  136. Peter,

    Environments change. And your bloviations do not amount to evidence.

    I will take my knowledge of evolution against yours, Peter.

    Longer legs are meaningless if you don’t have the muscles to make you go faster. Also the fastest is teh first to the lion’s ambush, duh.

  137. Peter,

    Every single one on Allan’s list is either a random mutation or how random mutations accumulate. Genetic regulation- all cobbled together via accumulations of random mutations.

    BTW changes in behaviour ruin evolution because it is easier to change behaviour to gain a reproductive advantage than it is waiting for some random genetic change to come about.

  138. 138

    Joe,

    Peter,

    Environments change.

    Sure. But usually not very fast. And organisms that can’t keep up, well they go extinct. Given that 99%+ of all species that existed no longer exist that’s the norm, eventually.

    I will take my knowledge of evolution against yours, Peter.

    Except that you don’t see to actually have any! You think that selection is irrelevant!

    Longer legs are meaningless if you don’t have the muscles to make you go faster. Also the fastest is teh first to the lion’s ambush, duh.

    You can create any scenario you like to try and nullify selection, but on average faster runners will be more likely to escape from a chasing lion. It’s a simple fact. And you can only leave descendants if you are alive!

    So sure, sometimes the fittest organism will get hit by a falling tree. Sometimes the fastest runner will run into an ambush rather then escape. But the other 99% of the time the fittest will survive and leave more descendants then the less fit.

    The fact that you try and dismiss selection in this way again just shows me how desperate you are to avoid really understanding evolution in any great depth.

    Oh, selection is meaningless because sometimes the most fit die?

    Risible!

  139. Since Upright and null are squirming to avoid it, are there any other ID proponents who would like to answer Nick’s simple question?

    With regard to information, the main question I’m interested in is, if a gene is duplicated, and one copy get modified such that it has a different specificity or function, has the amount of information in the genome increased?

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