Home » Darwinism, Evolution, Intelligent Design » Can You Say “WEASEL”?

Can You Say “WEASEL”?

Check out the following paper at arXiv. It gives yet another incarnation of Dawkins’ WEASEL. Let me suggest that Darwinists next try a horror version of it: “The WEASEL That Wouldn’t Die.” Perhaps Michael Moore can help make it. 

There’s plenty of time for evolution

Herbert S. Wilf
Department of Mathematics, University of Pennsylvania
Philadelphia, PA 19104-6395
[email protected]>

Warren J. Ewens
Department of Biology, University of Pennsylvania
Philadelphia, PA 19104-6018
[email protected]>

October 28, 2010

Abstract: Objections to Darwinian evolution are often based on the time required to carry out the necessary mutations. Seemingly, exponential numbers of mutations are needed. We show that such estimates ignore the effects of natural selection, and that the numbers of necessary mutations are thereby reduced to about K log L, rather than KL, where L is the length of the genomic “word,” and K is the number of possible “letters” that can occupy any position in the word. The required theory makes contact with the theory of radix-exchange sorting in theoretical computer science, and the asymptotic analysis of certain sums that occur there.

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58 Responses to Can You Say “WEASEL”?

  1. I have one simple question.

    How does science tell the difference between ‘natural selection’ and ‘artificial selection’? And wouldn’t any computer demonstration be artificial selection regardless?

  2. Did anyone notify Bill Gates about this breakthrough? :)

  3. Nice catch, Dr. Dembski. The imaginary form of evolution, where every novel feature can be built on a continuous, or near-continuous, gradient of mutations, continues to live. Unfortunately for natural evolutionists, it only exists on blogs, in journals and in imaginations. Congratulations on another proof of the validity of an imaginary form of evolution

  4. any comments on this item?

    http://www.guardian.co.uk/scie.....0/oct/06/1

    not directly on this topic, but purports to explain complexity

  5. The authors seem to look at the algorithm which you described as partitioned search in your paper with R. Marks Conservation of Information in Search – Measuring the Cost of Success. So, at least it isn’t about Dawkins’s weasel…

  6. es58, from the article:

    ‘Tinkering with an ancestral template is also a core idea research in developmental evolution, more commonly known as “evo-devo”: the morphology of animals — from jellyfish to fly to worm to fish to human — is built using the same basic genetic toolkit, subtly reorganised and redeployed to build the wing of a fly or the limb of a human.’

    The main problem with the paper is that it assumes genetic reductionism, the idea that Body-Plan morphogenesis is directly controlled by mutations to DNA, but genetic reductionism is shown to be false in the first place.

    notes:

    Cortical Inheritance: The Crushing Critique Against Genetic Reductionism – Arthur Jones – video
    http://www.metacafe.com/watch/4187488

    “Live memory” of the cell, the other hereditary memory of living systems – 2005
    Excerpt: To understand this notion of “live memory”, its role and interactions with DNA must be resituated; indeed, operational information belongs as much to the cell body and to its cytoplasmic regulatory protein components and other endogenous or exogenous ligands as it does to the DNA database. We will see in Section 2, using examples from recent experiments in biology, the principal roles of “live memory” in relation to the four aspects of cellular identity, memory of form, hereditary transmission and also working memory.
    http://www.sciencedirect.com/s.....3daa6bdef8

    The Gene Myth, Part II – August 2010
    Excerpt: So even with the same sequence a given protein can have different shapes and functions. Furthermore, many proteins have no intrinsic shape, taking on different roles in different molecular contexts. So even though genes specify protein sequences they have only a tenuous influence over their functions.,,, So, to reiterate, the genes do not uniquely determine what is in the cell, but what is in the cell determines how the genes get used.,,, Only if the pie were to rise up, take hold of the recipe book and rewrite the instructions for its own production, would this popular analogy for the role of genes be pertinent.
    http://darwins-god.blogspot.co.....rt-ii.html

    This inability for the DNA code to account for body plans is also clearly shown by extensive mutation studies to the DNA of different organisms which show ‘exceedingly rare’ beneficial morphological changes from mutations to the DNA code.

    The Origin of Biological Information and the Higher Taxonomic Categories – Stephen Meyer”Neo-Darwinism seeks to explain the origin of new information, form, and structure as a result of selection acting on randomly arising variation at a very low level within the biological hierarchy, mainly, within the genetic text. Yet the major morphological innovations depend on a specificity of arrangement at a much higher level of the organizational hierarchy, a level that DNA alone does not determine. Yet if DNA is not wholly responsible for body plan morphogenesis, then DNA sequences can mutate indefinitely, without regard to realistic probabilistic limits, and still not produce a new body plan. Thus, the mechanism of natural selection acting on random mutations in DNA cannot in principle generate novel body plans, including those that first arose in the Cambrian explosion.”
    http://eyedesignbook.com/ch6/eyech6-append-d.html

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

    This following video is a bit more clear for explaining exactly why mutations to the DNA do not control Body Plan morphogenesis, since the mutations are the found to be the ‘bottom rung of the ladder’ as far as the ‘higher levels of the layered information’ of the cell are concerned:

    Stephen Meyer on Craig Venter, Complexity Of The Cell & Layered Information
    http://www.metacafe.com/watch/4798685

    further notes:

    Hopeful monsters,’ transposons, and the Metazoan radiation:
    Excerpt: Viable mutations with major morphological or physiological effects are exceedingly rare and usually infertile; the chance of two identical rare mutant individuals arising in sufficient propinquity to produce offspring seems too small to consider as a significant evolutionary event. These problems of viable “hopeful monsters” render these explanations untenable.
    Paleobiologists Douglas Erwin and James Valentine

    “Yet by the late 1980s it was becoming obvious to most genetic researchers, including myself, since my own main research interest in the ‘80s and ‘90s was human genetics, that the heroic effort to find the information specifying life’s order in the genes had failed. There was no longer the slightest justification for believing that there exists anything in the genome remotely resembling a program capable of specifying in detail all the complex order of the phenotype (Body Plan).”
    Michael John Denton page 172 of Uncommon Dissent

    This lack of beneficial morphological novelty also includes the highly touted four-winged fruit fly mutations:

    …Advantageous anatomical mutations are never observed. The four-winged fruit fly is a case in point: The second set of wings lacks flight muscles, so the useless appendages interfere with flying and mating, and the mutant fly cannot survive long outside the laboratory. Similar mutations in other genes also produce various anatomical deformations, but they are harmful, too. In 1963, Harvard evolutionary biologist Ernst Mayr wrote that the resulting mutants “are such evident freaks that these monsters can be designated only as ‘hopeless.’ They are so utterly unbalanced that they would not have the slightest chance of escaping elimination through natural selection.” – Jonathan Wells
    http://www.evolutionnews.org/2.....footnote19

    Darwin’s Theory – Fruit Flies and Morphology – video
    http://www.youtube.com/watch?v=hZJTIwRY0bs

    Experimental Evolution in Fruit Flies (35 years of trying to force fruit flies to evolve in the laboratory fails, spectacularly) – October 2010
    Excerpt: “Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles.,,, “This research really upends the dominant paradigm about how species evolve,” said ecology and evolutionary biology professor Anthony Long, the primary investigator.
    http://www.arn.org/blogs/index.....ruit_flies

  7. es58 further notes:

    Many times evolutionists will mention evo-devo (Evolutionary Developmental Biology) to try to support the Darwinian claim that minor changes/mutations to DNA can drive major morphological novelty, yet, in this following comment, from a 2005 Nature review article, evolutionary geneticist Jerry Coyne expressed strong skepticism at the proposed mechanism of ‘gene switches’ for evo-devo:

    “The evidence for the adaptive divergence of gene switches is still thin. The best case involves the loss of protective armor and spines in sticklebacks, both due to changes in regulatory elements. But these elements represent the loss of traits, rather than the origin of evolutionary novelties…We now know that Hox genes and other transcription factors have many roles besides inducing body pattern, and their overall function in development – let alone in evolution – remains murky.”
    http://www.evolutionnews.org/2.....35931.html

    Here is a more thorough critique of evo-devo:

    Nature’s “Gems”: Microevolution Meets Microevolution – Casey Luskin – August 2010
    http://www.evolutionnews.org/2......html#more

    Here are many more lines of evidence arguing against any DNA mechanisms for body plan development, Evo-Devo included:

    Response to John Wise – October 2010
    Excerpt: But there are solid empirical grounds for arguing that changes in DNA alone cannot produce new organs or body plans. A technique called “saturation mutagenesis”1,2 has been used to produce every possible developmental mutation in fruit flies (Drosophila melanogaster),3,4,5 roundworms (Caenorhabditis elegans),6,7 and zebrafish (Danio rerio),8,9,10 and the same technique is now being applied to mice (Mus musculus).11,12 None of the evidence from these and numerous other studies of developmental mutations supports the neo-Darwinian dogma that DNA mutations can lead to new organs or body plans–because none of the observed developmental mutations benefit the organism.
    http://www.evolutionnews.org/2.....38811.html

    As well, recent ‘cloning studies’ give evidence against DNA/Genetic reductionism:

    “There is now considerable evidence that genes alone do not control development. For example when an egg’s genes (DNA) are removed and replaced with genes (DNA) from another type of animal, development follows the pattern of the original egg until the embryo dies from lack of the right proteins. (The rare exceptions to this rule involve animals that could normally mate to produce hybrids.) The Jurassic Park approach of putting dinosaur DNA into ostrich eggs to produce a Tyrannosaurus rex makes exciting fiction but ignores scientific fact.”
    The Design of Life – William Dembski, Jonathan Wells Pg. 50

    If that wasn’t enough, the Human Genome Project really put the last nail in the coffin for “Genetic Reductionism”:

    DNA: The Alphabet of Life – David Klinghoffer
    Excerpt: But all this is trivial compared to the largely unheralded insight gained from the Human Genome Project, completed in 2003. The insight is disturbing. It is that while DNA codes for the cell’s building blocks, the information needed to build the rest of the creature is seemingly, in large measure, absent. ,,,The physically encoded information to form that mouse, as opposed to that fly, isn’t there. Instead, “It is as if the ‘idea’ of the fly (or any other organism) must somehow permeate the genome that gives rise to it.”
    http://www.evolutionnews.org/2....._life.html

    This following video gives a glimpse of this ‘higher level’ information in action:

    Fearfully and Wonderfully Made – Glimpses At Human Development In The Womb – video
    http://www.metacafe.com/watch/4249713

  8. William Dembski:

    Thank you for bringing to our attention this really remarkable paper. It’s intellectual horror at its best. I am completely speechless.

  9. nullasalus:

    How does science tell the difference between ‘natural selection’ and ‘artificial selection’? And wouldn’t any computer demonstration be artificial selection regardless?

    In a sense, it is true that any computer model would be “artificial selection”.

    And yet, I believe that it is possibly to build a computer model which mimics true “natural eselection”. I have proposed the concept a couple of times here, but nobody seems to care.

    First, I will give explicit definitions of artificial selection and natural selection.

    a) Artificial selection is a selection of replicators arranged and structured by a designer.

    b) Natural selection is a form of selection entirely caused by the properties of the replicator in its natural environment.

    It is import to notice that, in natural selection, it is only the reproductiove advantage (in positive selection) or disadvantage (in negative selection) which selects, obviously in the context of the existing environment.

    Another important point is that the environment is in no way “aware” of the necessities of the replicators. It acts, s to say, “passively”. It has no specific information about how the replicaors work, replicate, live or die.

    That is true natural selection.

    Now, let’s go to artificial selection, like in so called evolutionary computer models.

    The problem with practically all of them is that they do not mimic natural selection at all. They are, invariably, forms of intelligent selection, that is of intelligent design.

    So, let’s define intelligent selection:

    c) Intelligent selectio: any form of artificiaòl selection where the designer is influenced by his knowledge of the properties of the replicator in designing the environment.

    What happens in intelligent selection is that the environment is more or less explicitly designed to be able to select a specific property, a property which in itself would not be able to be recognized by true natural selection, IOWs a property which in itself would never confer a reproductive advantage to the replicator in an unaware environment.

    The simplest form of ontelligent selection is the weasel and similar: here the designer introducts explicitly the solution in the system. If you look at the saftware defining the enviornment and its “fitness function”, you will find the weasel phrase somewhere.

    But there are cases where the designer favours a certain output more indirectly. I suppose that AVIDA is one of them.

    The Szvostak paper, on which I have abundantly commented here, is another example. A specific function, the ability to bind ATP, is chosen by the designer of the system, searched for, recognized and actively selected. That function, in that form, would never be recognized and selected in a true natural cellular environment.

    In this way, intelligent selection hugely increases the potentiality of natural selection. RV + intelligent selection can easily achieve most results. RV + NS can achieve almost nothing.

    So, is there a way to build a system with artificial selection which mimics NS, IOWs that is not “intelligent selection”?

    Yes, it is. It would go more or less this way.

    The designer chooses a priori a computer environment. Let’s say Windows 7.

    Then he designs simple replicators which can replicate in the system (spomething like simple computer viruses), using the system’s natural resources.

    The designer fixes some system in the replicator which causes completely random variation in the replicators.

    And then the designer does nothing more. He just waits

    He does not write any fitmess function. He does not program any specific environment to look for any specific property of the replicators.

    He waits.

    And occasionally, he just checks if new, more complex replicators have evolved, utilizing better the resources of the operating system thanks to the random mutations in their code.

    And if that happens, he can just check what those mutations are, if they are simple or complex, their complexity in bits, and if they have any tendency to become “steps” toward more complex functions.

    That would be a good simulation. Not natural selection, but artificial non intelligent selection.

    Why nobody seems interested to do simply that?

  10. This is too funny- they write computer programs and explanations yet they don’t have any evidence that genetic acidents can accumulate in such away as to give ise to functional multi-prt systems.

    There is lso a peer-reviewed paper abut the highly improbale act of getting two specified mutations.

    So what happens when 3 or more specified mutations are required?

    As for natural selection it is a rsult and doesn’t do anything.

  11. gpuccio,

    I’m in the middle of a very tough semester, but I want to delurk to point out that what you’re asking for has been implemented numerous times. One good place to start is Tom Ray’s Tierra program. There are many more sophisticated examples developed since then that model many aspects of modern evolutionary theory in exactly the way you describe.

  12. MathGrrl:

    I have considered in the past the Tierra program, and I believe you are absolutely wrong. But if you want to bring on the details to support your statement, I am willing to listen.

    And I am waiting for the “more sophisticated examples” too.

    Convince me (but please, don’t compromise your studies: there are priorities in life).

  13. MathGrll:

    I checked quickly about Tierra. The main point seems to me that it is a “virtual computer”. IOWs, here again the environment is set by the designer, and a very detailed analysis of the software would be needed to check how much additional information is incorporated into the system. But I leave that kind of work to Dembski and Marks.

    My point was very different. The designer must not design the system for his simulation. He must only design the replicators for an existing real system (I suggested Windows 7, but Linux would fit too). And obviously the mutation system, more or less adjustable. And nothing else. And the replicators should select themselves in that “natural” system, which has not been set by the designer of the experiment, and therefore is certainly “neutral”.

    Moreover, it seems that anyway the results of Tierra, whatever it is, are not so stunning. I quote from Wikipedia:

    “Mark Bedau and Norman Packard developed statistical method of classifying evolutionary systems and in 1997, Bedau et al. applied these statistics to Evita, an Artificial life model similar to Tierra and Avida, but with limited organism interaction, and no parasitism, and concluded that Tierra-like systems do not exhibit the open-ended evolutionary signatures of naturally evolving systems.[3]

    Russell K. Standish has measured the informational complexity of Tierran ‘organisms’, and has similarly found limited complexity growth in Tierran evolution.[4]”

    But I am always open to your contributions on the subject.

  14. gpuccio,

    Why should the simulation have to run on Windows or Linux? Those operating systems are designed for general purpose computing. The environment for a simulation is supposed to reflect aspects of reality in which we observe evolution working.

    What’s important is not the operating system of the simulation but that, as you note above, the environment provides no other feedback than relative fitness, just as the real world does. In particular, mutation and recombination must be independent of the environment. With those restrictions in place, the simulation reflects the essential aspects of reality necessary for evolutionary mechanisms to be demonstrated.

    I used to have a list of a many such simulations; I’ll try to dig it up over the next couple of days. In the meantime, Googling for “Santa Fe Institute”, “genetic algorithms”, and “artificial life” should get you a lot of examples. I believe there is a list on the Tierra website as well.

    I’ll close with emphasizing that my only purpose in hopping in here was to point out that systems like the one you describe have been implemented, by many researchers. I’d be curious to hear your thoughts on those you choose to investigate further.

  15. MathGrrl:

    The subject is certainly interesting, and I hope I have the time to investigate it better. Anyway, I thank you for your input.

    The point with Windows or Linux is that those systems have certainly not been conceived by the author of the simulation. That is the important requirement. The environment must not have been designed thinking of the simulation.

    Otherwise, it is really difficult to judge if there is no form of hidden information about the results to be obtained in the system. I don’t mean intentional.

    The authors of Avida were probably convinced that they were running a correct simulation, but Dembski and Marks have shown that this is not the case. Probably, even Dawkins was convinced that the Weasel was a fair example, when he wrote what he wrote.

    The fact is, the ideas of people, including scientists, about information, function and searches are really confused. I really find the work of Dembski very clarifying under that respect (and you may know that I don’t always agre with anything which Dembski says).

    So, a thorough investigation of a wholly designed system like Tierra, where the environment is virtual and conceived together with the replicators, would require a careful critical analysis of the software, which is not in my power to do.

    My suggestion to use a pre-existing environment would give the highest assurance of equity to the simulation. It would be like working in double blind. Many biases would be avoided.

    You say:

    “Those operating systems are designed for general purpose computing. The environment for a simulation is supposed to reflect aspects of reality in which we observe evolution working.”.

    No. First of all, no computer simulation can reflect a biological context. The purpose is not that. The purpose is to reflect the mathematical aspects of “evolution”.

    A general purpose operating system is the best equivalent, in computer environment, of the “general purpose” environment of a planet (unless you believe that that environment was designed for life, abd are a theistic evolutionst).

    But I think that simulations are created to test the simple materialist model of darwinian evolution, and not theistic evolutionism. We could conceive special simulations for that :)

    So, the environment has to be independent from the happenings of the replicators’destinies. A “general purpose” computing environment has all those requirements. It has resources, and rules. And they are “natural” resources and rules, not the special “soup” or virtual resources specifically designed in Tierra.

    If a replicator can reproduce and survive in Windows, and if it is allowed random variation, why shouldn’t it in time develop complex new functions? If the darwinian model is correct, I mean!

    But it won’t. A simple software program will never develop something like an ordering algorithm of 200 bits (or any similar complex function), which was not present in the original replicator, only as a result of random variation and true “natural selection”. Not in Windows, not in Linux. Never.

    This is not a dogma. It is a prediction. Ready to be falsified.

  16. es58:

    The interesting paper you link is a very good example of diversification in a single protein superfamily.

    That is completely in line with what I have argued many times, that continuity can be found only inside a functional island (a basic protein domain, or a superfamily). That is what is meant by the “big bang theory of proteins”.

    Fundamental protein superfamily appear independently, and then undergo limited variation in time inside the functional island.

    That’s why I always focus on the origin of protein superfamilies as the main point in the present ID debate.

    The following variation can be interpreted in two different ways:

    1) Neutral mutations can explore the functional island without significantly altering the function, while negative mutations are removed by negative selection. In this case, the function and folding remain the same.

    2) A diversification of specific subfunctions can be obtained through minor variations, usually at the level of the active site, while the main function and basic folding are retained.

    I think that the paper in question deals with this second aspect. In essence, these events are microevolutionary, and don’t require great variation of the molecule.

    We may ask: are these tweakings of function simple darwinian micrevolutionary events, or are they designed too?

    I don’t think we can answer that, at present. I confess that, for function diversifications like those described in the paper, which deal with complex regulatory systems, they are probably designed.

    The point is, the variation in the single molecule is probably not so great that it must necessarily fall into the design category (IOWs, it is not of the order of dFSCI). So, I don’t believe we can infer design on the basis of the events in the single molecule.

    But, if we could analyze the variation at system level, things would probably change, and design could be probably inferred.

    Anyway, as you probably know, I don’t even try to analyze complexity at system level. It is too big a challenge. I prefer at present to consider only the single molecule level.

    And so, back to our protein superfamilies…

  17. This paper is “proof by equivocation“. The phrase “natural selection” in the paper is not the same as natural selection in the wild.

    I should mention the remarkable feats being reported concerning the use of selection in computation to design shapes, robots and products using the likes of ‘genetic algorithms’. The claim here is that, given a complex shape coded for by several to many “genes”, a selection process can be instituted to improve any function imposed upon that shape. The resulting shape changes are not predictable (not built into the program to begin with), nor is the trajectory taken during the improvement. In other words, this models a multigene selection process. However, it does not escape Haldane’s dilemma, because there is only one function being selected at a time — one selection pressure. Perhaps two functions could be optimized simultaneously, given a large enough population of robots. This is not like selection among organisms, where only fitness is maximized, not any particular function. Another disanalogy can be seen when we note that much, if not most, genetic information in organisms is pleiotropic. This means that not just any old change that will improve some function can be selected in organisms without consequence for other functions. The selection model seems to work better in genetic algorithms than it could in organisms!

    Stanley Salthe

  18. gpuccio,

    As the old joke goes, “I think I see the problem.”

    From your post above:

    If a replicator can reproduce and survive in Windows, and if it is allowed random variation, why shouldn’t it in time develop complex new functions? If the darwinian model is correct, I mean!

    But it won’t. A simple software program will never develop something like an ordering algorithm of 200 bits (or any similar complex function), which was not present in the original replicator, only as a result of random variation and true “natural selection”. Not in Windows, not in Linux. Never.

    Why would you expect a new function to evolve in the absence of any selection pressure?

    This is exactly why any simulation of evolutionary mechanisms must run in a simulated environment rather than a general purpose operating system. Tierra, for example, provides an environment where the limited resources are RAM and clock cycles. The programs that evolve in that environment, via random mutation and recombination, demonstrate increasing efficiency in using those resources.

    While it should be possible to create an environment in which sorting algorithms evolve, there is no reason to expect it to happen in a general purpose OS where there is no benefit to doing so.

  19. Math Girl:

    Please excuse me for jumping into this conversation—I haven’t really looked at all the earlier posts, but I can’t help but note this:

    While it should be possible to create an environment in which sorting algorithms evolve, there is no reason to expect it to happen in a general purpose OS where there is no benefit to doing so.

    Isn’t this exactly the problem? How does one “create” an environment that ‘rewards’ certain configurations without inputting some selection functions? But this then means that human intelligence has to come up with a ‘reasonable’ selection function that will then operate under ‘reasonable’ conditions. This is information, located in an intelligent agent. How do you surmount this problem?

  20. MathGrrl:

    I don’t agree with you. Resources are limited everywhere, in a general purpose computer environment like in any other setting. Competition arises everywhere.

    Could you explain for example why bacteria would have evolved to eukaryotes and then to multicellular beings, when they still are the most successful reproductors on our planet?

    What environment favoured the more complex structures?

    I believe that everybpody emphasizes too much the concept of “selection pressure”. Maybe because the only real model of darwinism is antibiotic resistance? But you know, that is an extreme scenario.

    And then, isn’t RV the real originator of the new functions? RV knows nothing of selection pressure. If a new function arises by RV, it will be a new useful function also in a general purpose computer environment, I believe.

    Or shoud we believe that each new protein superfamily arose because of a new specific selection pressure in the environment? That would be an interesting concept.

    And the DNA code? Selection pressure that too?

  21. PaV,

    Hop right in, the water’s fine!

    Isn’t this exactly the problem? How does one “create” an environment that ‘rewards’ certain configurations without inputting some selection functions?

    While there are some GAs that use explicit fitness functions, in those like Tierra fitness is implicit in how well a program performs in the environment.

    But this then means that human intelligence has to come up with a ‘reasonable’ selection function that will then operate under ‘reasonable’ conditions. This is information, located in an intelligent agent. How do you surmount this problem?

    By not creating a fitness function! Tierra is about the simplest environment possible, given that RAM and time are the only two resources available. Programs live or die based on how well they use those resources. Interestingly, even in such a simple environment we see parasites evolve, and resistance to parasites, and “hyper parasites” that prey on the new programs.

  22. MathGirl:

    Here’s the other foot in the water!

    You said:

    ierra is about the simplest environment possible, given that RAM and time are the only two resources available. Programs live or die based on how well they use those resources.

    This type of programming seems harmless enough. But the devil is in the details. Viz., when you say that the programs “live or die based on how well they use those resources,” just what, exactly, determines “how well” they’re doing. Why kind of a comparison is involved? And who decided that this comparison is a good one to make?

  23. gpuccio,

    I don’t agree with you. Resources are limited everywhere, in a general purpose computer environment like in any other setting. Competition arises everywhere.

    That’s a good point. It should, in theory, be possible to create a version of Tierra that runs on a standard OS. It would look a lot like a very nasty software virus.

    Security issues aside, there is no logical difference between a simple simulation environment and Windows or Linux in this context, although the environments like Tierra’s do allow much easier monitoring. That’s quite important when doing research.

    Could you explain for example why bacteria would have evolved to eukaryotes and then to multicellular beings, when they still are the most successful reproductors on our planet?

    Well, that’s kind of off-topic, and also a bit inaccurate. Modern bacteria have evolved for just as long as every other modern organism. The general issue of the rise of multicellularity is an interesting topic, but definitely outside the scope of this discussion.

    What environment favoured the more complex structures?

    The real world. It;s must more complex than even our best computer simulations.

    I believe that everybpody emphasizes too much the concept of “selection pressure”.

    My point was that, unless it provides some survival benefit to the program, there is no reason to expect a sorting algorithm to evolve.

    Maybe because the only real model of darwinism is antibiotic resistance?

    You should know that is a grossly inaccurate statement.

    And then, isn’t RV the real originator of the new functions? RV knows nothing of selection pressure. If a new function arises by RV, it will be a new useful function also in a general purpose computer environment, I believe.

    It can only be “useful” in a particular context. If the only context is efficient utilization of RAM and clock cycles, a sorting algorithm is useless.

    Or shoud we believe that each new protein superfamily arose because of a new specific selection pressure in the environment? That would be an interesting concept.

    It would be more accurate to say that the alleles that result in those proteins arose over time via evolutionary mechanisms, providing benefit (or at least no significant disadvantages) at each iteration in the environment in which that iteration existed. This is evolutionary biology 101 — it should be understood by anyone participating in a discussion such as this.

  24. PaV,

    All of your questions can be answered from the Tierra overview on its website. Google “Tom Ray Tierra” for lots of links.

  25. Mathgrrl, pardon my intrusion, but perhaps you may be interested in this paper:

    LIFE’S CONSERVATION LAW – William Dembski – Robert Marks – Pg. 13
    Excerpt: Simulations such as Dawkins’s WEASEL, Adami’s AVIDA, Ray’s Tierra, and Schneider’s ev appear to support Darwinian evolution, but only for lack of clear accounting practices that track the information smuggled into them.,,, Information does not magically materialize. It can be created by intelligence or it can be shunted around by natural forces. But natural forces, and Darwinian processes in particular, do not create information. Active information enables us to see why this is the case.
    http://evoinfo.org/publication.....ation-law/

  26. Mathgrrl, I also noticed you made this unsubstantiated assumption:

    Modern bacteria have evolved for just as long as every other modern organism.

    Yet the best evidence we have says that no evolution has occurred in bacteria:

    The Paradox of the “Ancient” Bacterium Which Contains “Modern” Protein-Coding Genes:
    “Almost without exception, bacteria isolated from ancient material have proven to closely resemble modern bacteria at both morphological and molecular levels.” Heather Maughan*, C. William Birky Jr., Wayne L. Nicholson, William D. Rosenzweig§ and Russell H. Vreeland ;
    http://mbe.oxfordjournals.org/...../19/9/1637

    The oldest bacterium fossils, found on earth demonstrate an extreme conservation of morphology which, very contrary to evolutionary thought, simply means they have not changed and look very similar to bacteria of today.

    AMBER: THE LOOKING GLASS INTO THE PAST:
    Excerpt: These (fossilized bacteria) cells are actually very similar to present day cyanobacteria. This is not only true for an isolated case but many living genera of cyanobacteria can be linked to fossil cyanobacteria. The detail noted in the fossils of this group gives indication of extreme conservation of morphology, more extreme than in other organisms.
    http://bcb705.blogspot.com/200.....st_23.html

    Bacteria: Fossil Record – Ancient Compared to Modern – Picture
    http://www.ucmp.berkeley.edu/b.....riafr.html

    Was our oldest ancestor a proton-powered rock? – Oct. 2009
    Excerpt: “There is no doubt that the progenitor of all life on Earth, the common ancestor, possessed DNA, RNA and proteins, a universal genetic code, ribosomes (the protein-building factories), ATP and a proton-powered enzyme for making ATP. The detailed mechanisms for reading off DNA and converting genes into proteins were also in place. In short, then, the last common ancestor of all life looks pretty much like a modern cell.”
    http://www.newscientist.com/ar.....-rock.html

    as well, we now have concrete evidence for photosynthetic life suddenly appearing on earth, as soon as water appeared on the earth, in the oldest sedimentary rocks ever found on earth.

    The Sudden Appearance Of Photosynthetic Life On Earth – video
    http://www.metacafe.com/watch/4262918

    The oldest sedimentary rocks on earth, known to science, originated underwater (and thus in relatively cool environs) 3.86 billion years ago. Those sediments, which are exposed at Isua in southwestern Greenland, also contain the earliest chemical evidence (fingerprint) of ‘photosynthetic’ life [Nov. 7, 1996, Nature]. This evidence had been fought by materialists since it is totally contrary to their evolutionary theory. Yet, Danish scientists were able to bring forth another line of geological evidence to substantiate the primary line of geological evidence for photo-synthetic life in the earth’s earliest sedimentary rocks.

    U-rich Archaean sea-floor sediments from Greenland – indications of +3700 Ma oxygenic photosynthesis (2003)
    http://adsabs.harvard.edu/abs/2004E&PSL.217..237R

    Electron transport and ATP synthesis during photosynthesis – Illustration
    http://www.ncbi.nlm.nih.gov/bo.....iggrp.1672

    Evolution vs ATP Synthase – Molecular Machine – video
    http://www.metacafe.com/watch/4012706

    Moreover the first DNA code in life had to be at least as complex as the current DNA code found universally in life:

    “Because of Shannon channel capacity that previous (first) codon alphabet had to be at least as complex as the current codon alphabet (DNA code), otherwise transferring the information from the simpler alphabet into the current alphabet would have been mathematically impossible” Donald E. Johnson – Bioinformatics: The Information in Life

    Biophysicist Hubert Yockey determined that natural selection would have to explore 1.40 x 10^70 different genetic codes to discover the optimal universal genetic code that is found in nature. The maximum amount of time available for it to originate is 6.3 x 10^15 seconds. Natural selection would have to evaluate roughly 10^55 codes per second to find the one that is optimal. Put simply, natural selection lacks the time necessary to find the optimal universal genetic code we find in nature. (Fazale Rana, -The Cell’s Design – 2008 – page 177)

    DNA – The Genetic Code – Optimal Error Minimization & Parallel Codes – Dr. Fazale Rana – video
    http://www.metacafe.com/watch/4491422

    Mathgrrl I have a question for you, will you continue to claim bacteria have ‘always been evolving’ even though you have no evidence to substantiate your claim?

  27. BA, it appears the water got cold all of a sudden. What happened?

    Don’t tell me you brought another bucket of ice with you!? This isn’t the first time, you know!

    Darn it all, BA. You KNOW drive-bys like their tea hot! Better brush up on your manners.

    :)

  28. bornagain77,

    Mathgrrl, I also noticed you made this unsubstantiated assumption:

    Modern bacteria have evolved for just as long as every other modern organism.

    Yet the best evidence we have says that no evolution has occurred in bacteria:

    I’ve got a heavy load this semester, so I’m limiting my participation in this thread to discussion of GAs that meet gpuccio’s criteria.

    However, if you want to learn about the evolution of modern bacteria, you should read some actual textbooks and peer-reviewed papers. Your claim is completely at odds with a significant amount of empirical evidence.

  29. Orasmus,

    Is that an example of the civility expected of participants on this site?

  30. Actually MathGrrl I have cited some of the best empirical evidence available yet you state:

    ‘However, if you want to learn about the evolution of modern bacteria, you should read some actual textbooks and peer-reviewed papers.’

    Perhaps you are under the delusion that you actually have evidence for bacteria evolving? Well contrary to your claims the ACTUAL evidence is indeed a bucket of cold water on your fantasies of the continued evolution of bacteria throughout their history on earth:

    further notes on the best evidence we have for ancient bacteria:

    Some bacterium spores, in salt crystals, dating back as far as 250 million years have been revived, had their DNA sequenced, and compared to their offspring of today (Vreeland RH, 2000 Nature). To the disbelieving shock of many scientists, both ancient and modern bacteria were found to have the almost same exact DNA sequence.

    The Paradox of the “Ancient” Bacterium Which Contains “Modern” Protein-Coding Genes:
    “Almost without exception, bacteria isolated from ancient material have proven to closely resemble modern bacteria at both morphological and molecular levels.” Heather Maughan*, C. William Birky Jr., Wayne L. Nicholson, William D. Rosenzweig§ and Russell H. Vreeland ;
    http://mbe.oxfordjournals.org/...../19/9/1637

    Evolutionists were so disbelieving at this stunning lack of change that they insisted the stunning similarity was due to modern contamination in Vreeland’s experiment. Yet the following study laid that objection to rest by verifying that Dr. Vreeland’s methodology for extracting ancient DNA was solid and was not introducing contamination because the DNA sequences this time around were completely unique:

    World’s Oldest Known DNA Discovered (419 million years old) – Dec. 2009
    Excerpt: But the DNA was so similar to that of modern microbes that many scientists believed the samples had been contaminated. Not so this time around. A team of researchers led by Jong Soo Park of Dalhousie University in Halifax, Canada, found six segments of identical DNA that have never been seen before by science. “We went back and collected DNA sequences from all known halophilic bacteria and compared them to what we had,” Russell Vreeland of West Chester University in Pennsylvania said. “These six pieces were unique”,,,
    http://news.discovery.com/eart.....vered.html

    These following studies, by Dr. Cano on ancient bacteria, preceded Dr. Vreeland’s work:

    “Raul J. Cano and Monica K. Borucki discovered the bacteria preserved within the abdomens of insects encased in pieces of amber. In the last 4 years, they have revived more than 1,000 types of bacteria and microorganisms — some dating back as far as 135 million years ago, during the age of the dinosaurs.,,, In October 2000, another research group used many of the techniques developed by Cano’s lab to revive 250-million-year-old bacteria from spores trapped in salt crystals. With this additional evidence, it now seems that the “impossible” is true.”
    http://www.physicsforums.com/s.....p?t=281961

    Revival and identification of bacterial spores in 25- to 40-million-year-old Dominican amber
    Dr. Cano and his former graduate student Dr. Monica K. Borucki said that they had found slight but significant differences between the DNA of the ancient, 25-40 million year old amber-sealed Bacillus sphaericus and that of its modern counterpart,(thus ruling out that it is a modern contaminant, yet at the same time confounding materialists, since the change is not nearly as great as evolution’s ‘genetic drift’ theory requires.)
    http://www.sciencemag.org/cgi/...../5213/1060

    30-Million-Year Sleep: Germ Is Declared Alive
    http://query.nytimes.com/gst/f.....gewanted=2

    Dr. Cano’s work on ancient bacteria came in for intense scrutiny since it did not conform to Darwinian predictions, and since people found it hard to believe you could revive something that was millions of years old. Yet Dr. Cano has been vindicated:

    “After the onslaught of publicity and worldwide attention (and scrutiny) after the publication of our discovery in Science, there have been, as expected, a considerable number of challenges to our claims, but in this case, the scientific method has smiled on us. There have been at least three independent verifications of the isolation of a living microorganism from amber.”
    http://www.uncommondescent.com.....ent-357693

    In reply to a personal e-mail from myself, Dr. Cano commented on the ‘Fitness Test’ I had asked him about:
    Dr. Cano stated: “We performed such a test, a long time ago, using a panel of substrates (the old gram positive biolog panel) on B. sphaericus. From the results we surmised that the putative “ancient” B. sphaericus isolate was capable of utilizing a broader scope of substrates. Additionally, we looked at the fatty acid profile and here, again, the profiles were similar but more diverse in the amber isolate.”:
    Fitness test which compared ancient bacteria to its modern day descendants, RJ Cano and MK Borucki

    Thus, the most solid evidence available for the most ancient DNA scientists are able to find does not support evolution happening on the molecular level of bacteria. In fact, according to the fitness test of Dr. Cano, the change witnessed in bacteria conforms to the exact opposite, Genetic Entropy; a loss of functional information/complexity, since fewer substrates and fatty acids are utilized by the modern strains. Considering the intricate level of protein machinery it takes to utilize individual molecules within a substrate, we are talking an impressive loss of protein complexity, and thus loss of functional information, from the ancient amber sealed bacteria. Here is a revisit to the video of the ‘Fitness Test’ that evolutionary processes have NEVER passed as for a demonstration of the generation of functional complexity/information above what was already present in a parent species bacteria:

    Is Antibiotic Resistance evidence for evolution? – ‘Fitness Test’ – video
    http://www.metacafe.com/watch/3995248

    According to prevailing evolutionary dogma, there ‘HAS’ to be ‘major genetic drift’ to the DNA of bacteria within 250 million years, even though the morphology (shape) of the bacteria can be expected to remain exactly the same. In spite of their preconceived materialistic bias, scientists find there is no significant genetic drift from the ancient DNA. In fact recent research, with bacteria which are alive right now, has also severely weakened the ‘genetic drift’ argument of evolutionists:

    The consequences of genetic drift for bacterial genome complexity – Howard Ochman – 2009
    Excerpt: The increased availability of sequenced bacterial genomes allows application of an alternative estimator of drift, the genome-wide ratio of replacement to silent substitutions in protein-coding sequences. This ratio, which reflects the action of purifying selection across the entire genome, shows a strong inverse relationship with genome size, indicating that drift promotes genome reduction in bacteria.
    http://genome.cshlp.org/conten.....091785.109

    I find it interesting that the materialistic theory of evolution expects there to be a significant amount of genetic drift from the DNA of ancient bacteria to its modern descendants, while the morphology can be allowed to remain exactly the same with its descendants. Alas for the materialist once again, the hard evidence of ancient DNA has fell in line with the anthropic hypothesis.

  31. bornagain77,

    I apologize, but I simply don’t have time to engage with you on this topic. I encourage you to research the peer-reviewed literature rather than looking only at material that supports your preferred conclusion. You will find a truly enormous amount of empirical data regarding bacterial evolution.

    Enjoy.

  32. MathGrrl,

    Perhaps you mean Lenski’s long term experiment is this ‘overwhelming evidence’ you have for the evolution of bacteria?

    These following articles refute Richard E. Lenski’s ‘supposed evolution’ of the citrate ability for the E-Coli bacteria after 20,000 generations of the E-Coli from his ‘Long Term Evolution Experiment’ (LTEE) which has been going on since 1988:

    Multiple Mutations Needed for E. Coli – Michael Behe
    Excerpt: As Lenski put it, “The only known barrier to aerobic growth on citrate is its inability to transport citrate under oxic conditions.” (1) Other workers (cited by Lenski) in the past several decades have also identified mutant E. coli that could use citrate as a food source. In one instance the mutation wasn’t tracked down. (2) In another instance a protein coded by a gene called citT, which normally transports citrate in the absence of oxygen, was overexpressed. (3) The overexpressed protein allowed E. coli to grow on citrate in the presence of oxygen. It seems likely that Lenski’s mutant will turn out to be either this gene or another of the bacterium’s citrate-using genes, tweaked a bit to allow it to transport citrate in the presence of oxygen. (He hasn’t yet tracked down the mutation.),,, If Lenski’s results are about the best we’ve seen evolution do, then there’s no reason to believe evolution could produce many of the complex biological features we see in the cell.
    http://www.amazon.com/gp/blog/.....96N278Z93O

    Lenski’s e-coli – Analysis of Genetic Entropy
    Excerpt: Mutants of E. coli obtained after 20,000 generations at 37°C were less “fit” than the wild-type strain when cultivated at either 20°C or 42°C. Other E. coli mutants obtained after 20,000 generations in medium where glucose was their sole catabolite tended to lose the ability to catabolize other carbohydrates. Such a reduction can be beneficially selected only as long as the organism remains in that constant environment. Ultimately, the genetic effect of these mutations is a loss of a function useful for one type of environment as a trade-off for adaptation to a different environment.
    http://www.answersingenesis.or.....n-bacteria

    Even more crushing evidence can be gleaned from Lenski’s long term evolution experiment on E-coli. Upon even closer inspection, it seems Lenski’s ‘cuddled’ E. coli are actually headed for genetic meltdown instead of evolving into something, anything, better.

    New Work by Richard Lenski:
    Excerpt: Interestingly, in this paper they report that the E. coli strain became a “mutator.” That means it lost at least some of its ability to repair its DNA, so mutations are accumulating now at a rate about seventy times faster than normal.
    http://www.evolutionnews.org/2.....enski.html

    Lenski’s work actually did do something useful in that it proved that ‘convergent evolution’ is impossible because it showed that evolution is ‘historically contingent’. This following video and article make this point clear:

    Lenski’s Citrate E-Coli – Disproof of Convergent Evolution – Fazale Rana – video (the disproof of convergence starts at the 2:45 minute mark of the video)
    http://www.metacafe.com/watch/4564682

    The Long Term Evolution Experiment – Analysis
    Excerpt: The experiment just goes to show that even with historical contingency and extreme selection pressure, the probability of random mutations causing even a tiny evolutionary improvement in digestion is, in the words of the researchers who did the experiment, “extremely low.” Therefore, it can’t be the explanation for the origin and variety of all the forms of life on Earth.
    http://www.scienceagainstevolution.org/v12i11f.htm

    The loss of ‘convergent evolution’, as a argument for molecular sequence similarity, is a major blow to neo-Darwinian story telling:

    Implications of Genetic Convergent Evolution for Common Descent – Casey Luskin – Sept. 2010
    Excerpt: When building evolutionary trees, evolutionists assume that functional genetic similarity is the result of inheritance from a common ancestor. Except for when it isn’t. And when the data doesn’t fit their assumptions, evolutionists explain it away as the result of “convergence.” Using this methodology, one can explain virtually any dataset. Is there a way to falsify common descent, even in the face of convergent genetic similarity? If convergent genetic evolution is common, how does one know if their tree is based upon homologous sequences or convergent ones? Critics like me see the logic underlying evolutionary trees to be methodologically inconsistent, unpersuasive, and ultimately arbitrary.
    http://www.evolutionnews.org/2.....37841.html

    Origin of Hemoglobins: A Repeated Problem for Biological Evolution – 2010
    Excerpt: When analyzed from an evolutionary perspective, it appears as if the hemoglobins originated independently in jawless vertebrates and jawed vertebrates.,,, This result fits awkwardly within the evolutionary framework. It also contradicts the results of the Long-term Experimental Evolution (LTEE; Lenski) study, which demonstrated that microevolutionary biochemical changes are historically contingent.
    http://www.reasons.org/origin-.....-evolution

    Convergence: Evidence for a Single Creator – Fazale Rana
    Excerpt: When critically assessed, the evolutionary paradigm is found to be woefully inadequate when accounting for all the facets of biological convergence. On the other hand, biological convergence is readily explained by an origins model that evokes a single Creator (reusing optimal designs).
    http://www.reasons.org/converg.....le-creator

  33. Now dang it MathGrrl now you done really got me interested, just where is this conclusive evidence for bacteria generating information above what was already present?

    Reductive Evolution Can Prevent Populations from Taking Simple Adaptive Paths to High Fitness – Ann K. Gauger, Stephanie Ebnet, Pamela F. Fahey, and Ralph Seelke – 2010
    Excerpt: In experimental evolution, the best way to permit various evolutionary alternatives, and assess their relative likelihood, is to avoid conditions that rule them out. Our experiments, like others (e.g. [40]), used populations of cells growing slowly under limiting nutrient conditions, thereby allowing a number of paths to be taken to higher fitness. We engineered the cells to have a two-step adaptive path to high fitness, but they were not limited to that option. Cells could reduce expression of the non-functional trpAE49V,D60N allele in a variety of ways, or they could acquire a weakly functional tryptophan synthase subunit by a single site reversion to trpAD60N, bringing them within one step of full reversion (Figure 6). When all of these possibilities are left open by the experimental design, the populations consistently take paths that reduce expression of trpAE49V,D60N, making the path to new (restored) function virtually inaccessible. This demonstrates that the cost of expressing genes that provide weak new functions is a significant constraint on the emergence of new functions. In particular, populations with multiple adaptive paths open to them may be much less likely to take an adaptive path to high fitness if that path requires over-expression.
    http://bio-complexity.org/ojs/.....O-C.2010.2

    Response from Ralph Seelke to David Hillis Regarding Testimony on Bacterial Evolution Before Texas State Board of Education, January 21, 2009
    Excerpt: He has done excellent work showing the capabilities of evolution when it can take one step at a time. I have used a different approach to show the difficulties that evolution encounters when it must take two steps at a time. So while similar, our work has important differences, and Dr. Bull’s research has not contradicted or refuted my own.
    http://www.discovery.org/a/9951

  34. MathGrrl:

    I’ve looked at a powerpoint presentation of Tierra.

    First, we have intelligent agents intelligently trying to duplicate what they see in life on a logical framework. It is interesting that when it comes to trying to imitate life, so much logical thought is involved.

    Second, the entire program is setup in a very simplified way–very little complexity, and then it is set up so that nothing can really die, or, worse yet, cause the program itself to come to a halt. So, this program will live come hell or highwater.

    Third, from their results it looks like the only thing that has happened are: (1) the size of the program diminishes with time [akin to a loss of complexity], and (2) a “parasite” evolves. But the parasite is simply an organism that has lost its ability to copy its own program and so must rely on some other ‘cell’ to duplicate its ‘genome’. If one compares the “parasite” to the original “ancestor”, half of its instructions have been lost. So it seems that the upshot of this experiment in life via Darwinian processes results in a loss of size and a loss of complexity. This, of course, fits in perfectly with ID’s claims that claimed examples of Darwinian evolution generally amount to a loss of information and never a gain.

    I don’t see anything there in Tierra land that is of much interest. And apparently T.Ray doesn’t either since he worked on it from 1990-2001 and then quit.

  35. Dear Profs Wilf & Ewens:

    I went to bed with sweet dreams after ingesting your pleasant explanation of why “There’s plenty of time for evolution,” since ameliorative genomic changes are of course occurring in parallel throughout the entire population. Why didn’t I think of that before? I found the insight very reassuring and was able to fall into quite a refreshing slumber even without Ambien, in spite of the odious red tide of Republicans in the House.

    But now I have woken up in a cold sweat, for it occurred to me that these “favorable” changes must necessarily be occurring in individuals, not the species as a whole, at least initially. Individuals! Don’t you see? It’s Rush Limbaugh all over again. If we give individuals this kind of power, what happens to our beloved species? How can we work together for the sake of the collective and also embrace selfish individualism?

    Your theory conjures up a lovely vision of everyone striving in harmony to achieve positive change. But unless there’s something more than nature going on here, any positive genomic change that may occur by pure chance can only occur in specific individuals. They are not really working together. They are working for themselves. How in the world are we going to get them to share?

    After all, what are the chances that this heroic individual of ours will pass his positive genomic change—incrementally small as it must be and perhaps insignificant in itself—on to the entire species? We say his gene is naturally selfish, but then why would it want to share? Is it really true in nature that those who have are willing to share with those who have not?

    Actually just the opposite would seem to be true. In my pleasant dream, I see the whole busy community working together to improve themselves and sharing their positive genomic changes gladly. But in the acid etching of a starlit Republican night I see selfish individuals grabbing positive change for themselves and hoarding it to the grave.

    Do you see my dilemma? There is no capital gains tax in nature. How are we going to spread the wealth around? The industrious individual’s got it; who’s going to step in and make sure we get some of it? Without some way of forcing him to share, his positive genomic change perishes with him. Or is this miraculous sharing what you mean by “natural selection”? Are there loaves and fishes in nature?

    I know how much our side loves sex—but does it really help us here? What are the chances that a favorable genomic change will spread from one individual to an entire species, be he as generous with his lifeforce as Wilt Chamberlain himself? And remember, we are talking about only one small change! The same thing has to happen with every single ameliorative change that is needed in order to raise nightingales from the mire! (Let’s not even think about negative changes!)

    Please do write another paper soon and put this demon to rest. I’m having enough trouble sleeping as it is with these troglodyte Teabaggers clogging up the airwaves and forcing me to defend my esoteric wisdom. I know it must pain you to have to cast your pearls before swine, but do send us pleasant dreams as soon as you can.

    And in the meantime, keep the faith!

    Yours truly,
    Sir Richard

  36. Hello MathGrrl,

    Is it possible that you are the one who is “looking only at material that supports your preferred conclusion”, not bornagain77?

    It says so much about evolutionist beliefs that the best (only?) evidence they have these days is bacteria. We will all come to realise that bacteria actually presents the best evidence against evolution. Here’s why:

    Bacteria is believed to have been in existence for 3,000,000,000 years. It has the ability to asexually reproduce so quickly that populations can double in size every 10 minutes. It thrives in all environments, extreme or otherwise. It obtains genetic information from plasmids, bacteriophages, mutations and even other bacteria (no matter how distantly related they may be). There are about 5,000,000,000,000,000,000,000,000,000,000 of them on the planet today. With so many features to facilitate evolution, bacteria should have given rise to a multitude of species: things like flowers, fish, trees, whales, fungi, mice, canaries, dinosaurs, humans, etc. Yet not even a bacterial worm has been yielded in all this time.

    Surely people like MathGrrl cannot reflect upon this without feeling disturbed.

  37. @mathgrrl

    I also don’t think Tierra is very useful. The kind of thing that would interest me would be if the program could develop some kind of new function by itself. A scenario as follows comes to mind.

    Suppose we setup an environment within a virtual environment. where life forms (programs) consume food (image files).

    - Each program is allocated a portion of time per cycle in which to ‘digest’ – convert the image into its raw colour grid – food.

    - Each program has a limited number of cycles to operate i.e. it dies.

    - Food is introduced into the environment at a rate proportional, but not linearly, to the number of programs in the system.

    - Food image files comes in different types(formats) e.g. .bmp .gif, .jpeg, png, but also vector formats. Initially programs will only be able to digest .bmp files.

    - The different types of food will be introduced into the environment in different proportions and different times.

    - Programs could mutate in any random way. So to start with they have a single function which does all the work of reading and converting image files to the matrix in memory i.e. a two dimensional array. Mutation will allow copies of the function to be created and mutated i.e. random code insertions, deletions etc. Functions may also be copied from other programs. These functions could then be used via a mutated function call.

    The idea is that programs must compete for food. The more efficiently they can process the image the more food they can consume. The more food they have the more they can propogate. They have three ways of evolving. The can develop new efficiency around processing an image type. They can also develop ability to decode new bitmap formats. Lastly they can develop the ability to convert vector images into bitmap images, and then of course develop the ability to process a number of vector formats.

    If this or something similar was demonstrated I could believe evolution of new traits, features was possible through naturalistic processes.

  38. Chris Doyle@36

    I am not someone who believes evolution – at the very least naturalistic evolution, there may be a designed evolutionary system hidden somewhere in the cell we don’t know about – can account for the development of life.

    But how do we know there is no bacterial worm. Lets say bacteria did evolve from a single celled life form, how would we know that i.e. what would we look for?

    The same point can be made whenever we talk about beneficial mutations. We always say we have never seen one, but how do we know that. Surely it is much easier to spot a bad mutation than a good one. When we see a good one we may just assume it was always there.

    So I am asking how can one look at a genome and determine beneficial mutations. The other side is claiming pretty much everything in the genome is a beneficial mutation. None of us can prove it was or was not a mutation.

    Or am I missing something?

  39. allanius per the selfish individuals @ 35

    http://www.facebook.com/photo......0088262100

  40. Hi Andrew,

    You asked:

    “But how do we know there is no bacterial worm. Lets say bacteria did evolve from a single celled life form, how would we know that i.e. what would we look for?”

    In this case, we can rule out the possibility that a bacteria evolved into a worm (or anything else for that matter) by looking at the cells of the organism in question. Allow me to explain.

    The most fundamental distinction in organisms is the distinction between eukaryotes (whose cells contain a nucleus and other complex structures) and prokaryotes (whose cells don’t contain these things). All life on Earth consists of eukaryotes… apart from bacteria. Therefore, evolutionists believe that the first major fork in life involved all life on Earth (eukaryotes) going one way and bacteria (prokaryotes) going the other (up to 2.7 billion years ago). Bacteria today are all still microscopic organisms with a nucleoid, cytoplasm and ribosomes with-in a membrane, with-in a cell wall with-in an enclosing capsule. Pili protrude from the membrane and a flagellum provides motility. There is some trivial variation. Bacteria come in some different shapes and sizes. Different bacteria eat different things. Different bacteria are destroyed by different things. But that’s it. There are no bacterial flowers, fish, trees, whales, fungi, mice, canaries, dinosaurs, humans, etc.

    So, although evolutionists can claim that a worm evolved from a single celled eukaryotic ancestor, they cannot claim that a worm evolved from bacteria. The big question is, if evolution is true, why is it that we don’t have things like prokaryotic worms?

    As for beneficial mutations, I would appeal to Stephen Meyer’s “Signature in the Cell” which demonstrates that it is not a question of whether or not a beneficial mutation can be observed at any point in time but rather that the probablistic resources required for a random beneficial mutation to occur in the first place vastly exceed those on offer by the entire universe!

  41. MathGrrl (#23):

    First of all, I really don’t want to interfer with your duties, so I will comment on some of your points, but please feel completely free to answer ot not, according to the time you can use. We can always take again the discussion at another moment :).

    So, here are some thoughts.

    That’s a good point. It should, in theory, be possible to create a version of Tierra that runs on a standard OS. It would look a lot like a very nasty software virus.

    Well, I will be really interested if someone does that. And we can see how much complexity evolves.

    Security issues aside, there is no logical difference between a simple simulation environment and Windows or Linux in this context, although the environments like Tierra’s do allow much easier monitoring. That’s quite important when doing research.

    Well, I suppose that it sould be easy enough to monitor a virus which replicates throughout the system.

    Anyway, again my point is that using a pre-existem system, which has not been set by the experimenter, we have the only possible guarantee that no hidden information is introduced in the system.

    Anyway, if people that I have faith in, like Dembski and Marks, examine the Tierra system, an conclude that it is fair, and that no hidden information can be found in it, I will accept their judgement.

    And anyway, again, it seems, at least according to Wikipedis, that the system has generated no real complexity, so why bother?

    Well, that’s kind of off-topic, and also a bit inaccurate. Modern bacteria have evolved for just as long as every other modern organism. The general issue of the rise of multicellularity is an interesting topic, but definitely outside the scope of this discussion.

    And we will not discuss it, then.

    Regarding bacteria, as you can see if you look at my statement, I have never said that they have not evolved. I have asked why should they have evolved to eukaryotes or to multicellular beings, given their very successful reproduction rate.

    And about bacterial evolution, I would like anyway to make a point. I agree that bacteria have “evolved” in 4 billion years: there are certainly differences between modern bacteria and original ones. But my point is, we have no reason to believe that ancient bacteria had not already most of the functionality we observe today.

    Indeed, we have reason to believe the opposite.

    Going back to my favourite argument, the emergence of basic protein information in the form of protein superfamilies, I sum here the most likely scenario, according to current research (non ID):

    The last SCOP classification includes 1962 superfamilies.

    Of these, about half seem to have been already present in LUCA, and therefore in ancient bacteria and archea.

    The remaining half has emerged after, both in bacteria and in higher beings.

    I think there is no doubt that original bacteria and archea has already a great complexity, and were already very succsessful replicators.

    And please remember that most of what is labeled as “evolution” is modification inside an existing superfamily (see my answer to es58 at #16).

    The real world. It;s must more complex than even our best computer simulations.

    Maybe. But the important point is that its complexity is completely random (unrelated) in reference to the replicators. Again, unless you are a theist evolutionist. Or a strong IDist.

    In the same way, the environment in the simulation must be, beyond any possible bias, unrelated to the replicators.

    Then we can see if it is true that complex functional structures may emerge from an unrelated environment, however complex.

    My point was that, unless it provides some survival benefit to the program, there is no reason to expect a sorting algorithm to evolve.

    But again, it is certainly possible to have replicators which utilize better the resources of the operating system through complex functions. For instance, the designer could write better replicators which compete with the simpler ones, or with the exisitng programs and functions in the operationg system. Have you ever heard of spyware?

    A sorting algorithm nay be useful to such an “evolved” replicator ot not. Usually, sorting algorithms are very useful in a lot of programming situations, that’s why I mentioned it. But I said: a sorting algorithm or anything of similar complexity.

    There are a lot of complex ways that a software replicator can use to compete in a general purpose operating system. Virus programmers know that very well.

    The problem is that many of those strategies are indeed complex. My only point is: can they emerge from random variation and spontaneous, truly “natural” selection?
    My answer is: no. And again, I am waiting that it be falsified.

    It can only be “useful” in a particular context. If the only context is efficient utilization of RAM and clock cycles, a sorting algorithm is useless.

    I would not be so sure that a sorting algorithn cannpot be useful to utilize efficiently the resources of an operating system. We should ask a programmer. And anyway, as I have said, I have no special commitment to sorting algorithm. Any kind of new complex function will do. As darwinists always say, evolution can use any possible way to implement its (non existing) aims.

    You should know that is a grossly inaccurate statement.

    I don’t think so. But just to be cooperative, I could say that darwinism has just a few semidetailed microevolutionary models, of which antibiotic resistance is certainly the best understood and detailed. And the others are anyway very similar (simple mutations and extreme environmentsl pressure).

    I am aware of no detailed or credible model of macroevolution.

    But again, if you want to refere to any specific model, we can discuss it.

    It would be more accurate to say that the alleles that result in those proteins arose over time via evolutionary mechanisms, providing benefit (or at least no significant disadvantages) at each iteration in the environment in which that iteration existed. This is evolutionary biology 101 — it should be understood by anyone participating in a discussion such as this.

    We have absolutely no evidence that new protein superfamilies resulted “over time via evolutionary mechanisms”.

    A transition to a new superfamily from an existing superfamily bears the burden of a random search of the whole informational content of the new function, because the “original” superfamily is by definition an unrelated state, and no such transition has been deconstructed into discrete functional intermediates, not is there any evidence in the proteome of such intermediates.

    Therefore, the emergence of a new superfamily implies, as far as we know, the generation of new dFSCI, which cannot happen through a random search.

    The iterations you speak of are simply non existent in the proteome, and never modeled, not even theoretically.

    They are, for all purposes, a myth.

    And I must maybe remind you that only iterations which “provide (significant) benefit” can be (sometimes) fixed by NS (and would be one of those intermediate steps which don’t exist), while iterations which bear “no significant disadvantage” cannot be fixed, if not randomly by genetic drift, and therefore do not change at all the burden of the random search.

    I don’t know if this is biology 101, but it is simply true.

  42. Chris Doyle@40

    Thanks.

    Regarding the beneficial mutation and the resources available etc. I agree but I refer specifically to the argument which is often given i.e. that we have never observed a beneficial mutation. My point is we would not know directly even if one did occur because we would not be able to identify it directly. We can always detect the ones that aren’t beneficial because they break things and occur more frequently. So to me it seems that it is not an argument we should be making.

    Regarding the prokaryote worm. Wouldn’t the evolutionist just say they are not possible i.e. multi-celled organisms require eukaryotic cells. Would they not just say the evolutionary path was from bacteria to single celled eukaryotic organisms and then to multi-celled organisms?

  43. andrewjg:

    I would say that we see simple mutations in the genomes and proteomes. Most of them are apparently neutral, many are detrimental (human mendelian diseases are an example), and very rarely we see simple mutations which seem to bear some relative advantage (antibiotic resistance

  44. andrewjg:

    I would say that we see simple mutations in the genomes and proteomes. Most of them are apparently neutral, many are detrimental (human mendelian diseases are an example), and very rarely we see simple mutations which seem to bear some relative advantage (antibiotic resistance in bacteria, some small variations in existing enzymes, and so on).

    Almost all of hese examples are single mutations.

    Behe has discussed cloroquine resistence in the malaria parasite as a rare example of a two aminoacid “beneficial” mutation.

    Now, I am not discussing here if these mutations are truly “beneficial” (BA, please, take notice): I am just describing mutations which, in particular environments, can be selected and expanded.

    These are the mutations we can observe “in the making”.

    The rest we have to infer from genomes and proteomes.

    In proteomes, we see protein superfamilies which can retain the same function for billions of years, or which can “tweak” it a little to adapt new specific functions. And at the same time we see completely new protein superfamilies, folds and functions “emerge”, without any explenation.

    It is difficult to explain these observations on the basis of the few microevolutionary models we have, as I have tried to argue many times.

    Especially the existence of the 2000 basic protein superfamilies is at present the most detailed evidence of design in the proteome.

  45. andrewjg:

    Regarding the prokaryote worm. Wouldn’t the evolutionist just say they are not possible i.e. multi-celled organisms require eukaryotic cells. Would they not just say the evolutionary path was from bacteria to single celled eukaryotic organisms and then to multi-celled organisms?

    Yes, they would say that. And yet, I believe that Chris has raised an interesting point. Maybe prokaryotes are not good at building multicellular beings, but I don’t think we really understand why.

    The transition from prokaryotes to eukaryotes remains one of the mysterious “acute events” in evolution that defy any detailed explanation (others are obviously OOL, the origin of multicellularity and the Ediacara and Cambrian explosions).

  46. gpuccio@43

    To my mind antibiotic resistance would be classified as neutral. When I think of a beneficial mutation I am thinking of a mutation which perhaps when combined with other mutations can aggregate to create some kind of enhancement or new feature/function.

    So in the long run neutral mutations could be positive when combined with other neutral mutations. All this is theoretical I know. Purely from statistical reasoning I don’t believe you can just randomly change things and get to anything useful, at least not of sufficient combined complexity.

  47. gpuccio@44

    Thanks. One thing I wish was discussed more was the whole regulatory issue. I mean everyone talks about proteins because they are like parts/machines, but just as important is how and when these parts are used together to build more complex structures.

    I mean it is one thing to have the tools and the parts, it is another thing to know how and when to combine them to create something new, and when to use them.

    I think mutations to regulatory areas of the genome would be the most devastating and therefore error prevention, detection and correction would be the most critical and yet they would also have to have positive mutations for evolution to work.

  48. gpuccio you state:

    ‘We have absolutely no evidence that new protein superfamilies resulted “over time via evolutionary mechanisms”

    to which I might like to add that we have absolutely no evidence that existing proteins can ‘randomly’ vary, even a modest amount, even within their existing ‘superfamily’.

    What makes matters much worse for the materialist is that he will try to assert that existing functional proteins of one structure can easily mutate into other functional proteins, of a completely different structure or function, by pure chance. Yet once again the empirical evidence betrays the materialist. The proteins that are found in life are shown to be highly constrained in their ability to evolve into other proteins:

    Dollo’s law, the symmetry of time, and the edge of evolution – Michael Behe – Oct 2009
    Excerpt: Nature has recently published an interesting paper which places severe limits on Darwinian evolution.,,,
    A time-symmetric Dollo’s law turns the notion of “pre-adaptation” on its head. The law instead predicts something like “pre-sequestration”, where proteins that are currently being used for one complex purpose are very unlikely to be available for either reversion to past functions or future alternative uses.
    http://www.evolutionnews.org/2.....f_tim.html

    Severe Limits to Darwinian Evolution: – Michael Behe – Oct. 2009
    Excerpt: The immediate, obvious implication is that the 2009 results render problematic even pretty small changes in structure/function for all proteins — not just the ones he worked on.,,,Thanks to Thornton’s impressive work, we can now see that the limits to Darwinian evolution are more severe than even I had supposed.
    http://www.evolutionnews.org/2......html#more

    “Mutations are rare phenomena, and a simultaneous change of even two amino acid residues in one protein is totally unlikely. One could think, for instance, that by constantly changing amino acids one by one, it will eventually be possible to change the entire sequence substantially… These minor changes, however, are bound to eventually result in a situation in which the enzyme has ceased to perform its previous function but has not yet begun its ‘new duties’. It is at this point it will be destroyed – along with the organism carrying it.” Maxim D. Frank-Kamenetski, Unraveling DNA, 1997, p. 72. (Professor at Brown U. Center for Advanced Biotechnology and Biomedical Engineering)

    “A problem with the evolution of proteins having new shapes is that proteins are highly constrained, and producing a functional protein from a functional protein having a significantly different shape would typically require many mutations of the gene producing the protein. All the proteins produced during this transition would not be functional, that is, they would not be beneficial to the organism, or possibly they would still have their original function but not confer any advantage to the organism. It turns out that this scenario has severe mathematical problems that call the theory of evolution into question. Unless these problems can be overcome, the theory of evolution is in trouble.”
    Problems in Protein Evolution:
    http://www.cs.unc.edu/~plaisted/ce/blocked.html

    Extreme functional sensitivity to conservative amino acid changes on enzyme exteriors – Doug Axe
    Excerpt: Contrary to the prevalent view, then, enzyme function places severe constraints on residue identities at positions showing evolutionary variability, and at exterior non-active-site positions, in particular.
    http://nsmserver2.fullerton.ed.....lution.pdf

    As well, the ‘errors’ that are found in protein sequences are found to be ‘designed errors’:

    Cells Defend Themselves from Viruses, Bacteria With Armor of Protein Errors – Nov. 2009
    Excerpt: These “regulated errors” comprise a novel non-genetic mechanism by which cells can rapidly make important proteins more resistant to attack when stressed,
    http://www.sciencedaily.com/re.....134701.htm

    There are even ‘protein police’:

    GATA-1: A Protein That Regulates Proteins – Feb. 2010
    http://darwins-god.blogspot.co.....teins.html

    Heat shock proteins:
    Excerpt: They play an important role in protein-protein interactions such as folding and assisting in the establishment of proper protein conformation (shape) and prevention of unwanted protein aggregation. http://en.wikipedia.org/wiki/Heat_shock_protein

    This following paper, and audio interview, shows that there is a severe ‘fitness cost’ for cells to carry ‘transitional’ proteins that have not achieved full functionality yet:

    Reductive Evolution Can Prevent Populations from Taking Simple Adaptive Paths to High Fitness – May 2010
    Excerpt: Despite the theoretical existence of this short adaptive path to high fitness, multiple independent lines grown in tryptophan-limiting liquid culture failed to take it. Instead, cells consistently acquired mutations that reduced expression of the double-mutant trpA gene. Our results show that competition between reductive and constructive paths may significantly decrease the likelihood that a particular constructive path will be taken.
    http://bio-complexity.org/ojs/.....O-C.2010.2

    Testing Evolution in the Lab With Biologic Institute’s Ann Gauger – audio
    http://www.idthefuture.com/201.....lab_w.html

    In fact the Ribosome, which makes the myriad of different, yet specific, types of proteins found in life, is found to be severely intolerant to any random mutations occurring to proteins.

    The Ribosome: Perfectionist Protein-maker Trashes Errors
    Excerpt: The enzyme machine that translates a cell’s DNA code into the proteins of life is nothing if not an editorial perfectionist…the ribosome exerts far tighter quality control than anyone ever suspected over its precious protein products… To their further surprise, the ribosome lets go of error-laden proteins 10,000 times faster than it would normally release error-free proteins, a rate of destruction that Green says is “shocking” and reveals just how much of a stickler the ribosome is about high-fidelity protein synthesis.
    http://www.sciencedaily.com/re.....134529.htm

  49. gpuccio you state:

    ‘We have absolutely no evidence that new protein superfamilies resulted “over time via evolutionary mechanisms”

    to which I might like to add that we have absolutely no evidence that existing proteins can ‘randomly’ vary, even a modest amount, even within their existing ‘superfamily’.

    What makes matters much worse for the materialist is that he will try to assert that existing functional proteins of one structure can easily mutate into other functional proteins, of a completely different structure or function, by pure chance. Yet once again the empirical evidence betrays the materialist. The proteins that are found in life are shown to be highly constrained in their ability to evolve into other proteins:

    Dollo’s law, the symmetry of time, and the edge of evolution – Michael Behe – Oct 2009
    Excerpt: Nature has recently published an interesting paper which places severe limits on Darwinian evolution.,,,
    A time-symmetric Dollo’s law turns the notion of “pre-adaptation” on its head. The law instead predicts something like “pre-sequestration”, where proteins that are currently being used for one complex purpose are very unlikely to be available for either reversion to past functions or future alternative uses.
    http://www.evolutionnews.org/2.....f_tim.html

    Severe Limits to Darwinian Evolution: – Michael Behe – Oct. 2009
    Excerpt: The immediate, obvious implication is that the 2009 results render problematic even pretty small changes in structure/function for all proteins — not just the ones he worked on.,,,Thanks to Thornton’s impressive work, we can now see that the limits to Darwinian evolution are more severe than even I had supposed.
    http://www.evolutionnews.org/2......html#more

    “Mutations are rare phenomena, and a simultaneous change of even two amino acid residues in one protein is totally unlikely. One could think, for instance, that by constantly changing amino acids one by one, it will eventually be possible to change the entire sequence substantially… These minor changes, however, are bound to eventually result in a situation in which the enzyme has ceased to perform its previous function but has not yet begun its ‘new duties’. It is at this point it will be destroyed – along with the organism carrying it.” Maxim D. Frank-Kamenetski, Unraveling DNA, 1997, p. 72. (Professor at Brown U. Center for Advanced Biotechnology and Biomedical Engineering)

    “A problem with the evolution of proteins having new shapes is that proteins are highly constrained, and producing a functional protein from a functional protein having a significantly different shape would typically require many mutations of the gene producing the protein. All the proteins produced during this transition would not be functional, that is, they would not be beneficial to the organism, or possibly they would still have their original function but not confer any advantage to the organism. It turns out that this scenario has severe mathematical problems that call the theory of evolution into question. Unless these problems can be overcome, the theory of evolution is in trouble.”
    Problems in Protein Evolution:
    http://www.cs.unc.edu/~plaisted/ce/blocked.html

    Extreme functional sensitivity to conservative amino acid changes on enzyme exteriors – Doug Axe
    Excerpt: Contrary to the prevalent view, then, enzyme function places severe constraints on residue identities at positions showing evolutionary variability, and at exterior non-active-site positions, in particular.
    http://nsmserver2.fullerton.ed.....lution.pdf

    As well, the ‘errors’ that are found in protein sequences are found to be ‘designed errors’:

    Cells Defend Themselves from Viruses, Bacteria With Armor of Protein Errors – Nov. 2009
    Excerpt: These “regulated errors” comprise a novel non-genetic mechanism by which cells can rapidly make important proteins more resistant to attack when stressed,
    http://www.sciencedaily.com/re.....134701.htm

    This following paper, and audio interview, shows that there is a severe ‘fitness cost’ for cells to carry ‘transitional’ proteins that have not achieved full functionality yet:

    Reductive Evolution Can Prevent Populations from Taking Simple Adaptive Paths to High Fitness – May 2010
    Excerpt: Despite the theoretical existence of this short adaptive path to high fitness, multiple independent lines grown in tryptophan-limiting liquid culture failed to take it. Instead, cells consistently acquired mutations that reduced expression of the double-mutant trpA gene. Our results show that competition between reductive and constructive paths may significantly decrease the likelihood that a particular constructive path will be taken.
    http://bio-complexity.org/ojs/.....O-C.2010.2

    Testing Evolution in the Lab With Biologic Institute’s Ann Gauger – audio
    http://www.idthefuture.com/201.....lab_w.html

    In fact the Ribosome, which makes the myriad of different, yet specific, types of proteins found in life, is found to be severely intolerant to any random mutations occurring to proteins.

    The Ribosome: Perfectionist Protein-maker Trashes Errors
    Excerpt: The enzyme machine that translates a cell’s DNA code into the proteins of life is nothing if not an editorial perfectionist…the ribosome exerts far tighter quality control than anyone ever suspected over its precious protein products… To their further surprise, the ribosome lets go of error-laden proteins 10,000 times faster than it would normally release error-free proteins, a rate of destruction that Green says is “shocking” and reveals just how much of a stickler the ribosome is about high-fidelity protein synthesis.
    http://www.sciencedaily.com/re.....134529.htm

  50. andrejg:

    So in the long run neutral mutations could be positive when combined with other neutral mutations. All this is theoretical I know. Purely from statistical reasoning I don’t believe you can just randomly change things and get to anything useful, at least not of sufficient combined complexity.

    And you are perfectly right.

    The reasoning is simple. A neutral mutation happens in one individual, and remains confined to that individual (and its progeny). So, unless the population is rapidly expanding, the mutation will remain confined to a tiny minority of individuals (or will be just randomly lost).

    Therefore, if another neutral mutation which is necessary for the final function has to accumulate together with the first, it must happen in that single clone. Therefore, you have to multiply probabilities.

    That’s way even a two mutations dependent function (like cloroquine resistance in the malaria parasite) is so rare.

    One mutation variations are quite common, and they can be selected positively or negatively, if the emvironment allows that.

    Two mutation variations are really rare.

    My threshold for dFSCI in a biological system is 150 bits, which would be a functionally coordinated variation of 35 aminoacids. I am sure that such an event can never happen in a random biological system.

    But still, that is raising the bar just to be absolutely sure. I am sure that three aminoacid coordinated mutations are already so rare that they are the exception.

    Another thing has to be considered: all these numbers (Behe’s data from the malaria parasite, my threshold of 150 bits) are however derived form bacterial or single cell eukaryotes systems. That means huge populations and very high reproduction rates.

    Those same numbers are really ridicule in higher animals, where even a three aminoacid functional variation is probably completely out of the range.

  51. andrewjg:

    I mean it is one thing to have the tools and the parts, it is another thing to know how and when to combine them to create something new, and when to use them. I think mutations to regulatory areas of the genome would be the most devastating and therefore error prevention, detection and correction would be the most critical and yet they would also have to have positive mutations for evolution to work.

    And again you are perfectly right.

    But the problem is of two kinds:

    a) The nature of the regulatory system is much less understood than the nature of protein coding genes

    b) It is extremely more difficult to compute functional complexity in a system than in a single protein. Dembski has tried in the flagellum, but I am not sure that the result was really convincing.

    The reason is that in a system where many parts interact and are regulated, it is prohibitve to model correctly the functional space and the search space. So, it is difficult to be quantitative.

    Obviously, even a semi quantitative approach shows that the functional complexity of a system, and especially of a regulatory system, must be much higher than the simple sum of the complexity of its parts. I believe that the modeling of complex and regulatory systems will be the new frontier of ID theory.

    But for the moment, darwinists still have to explain how protein superfamilies emerged.

  52. BA77:

    you quoted:

    The Ribosome: Perfectionist Protein-maker Trashes Errors
    Excerpt: The enzyme machine that translates a cell’s DNA code into the proteins of life is nothing if not an editorial perfectionist…the ribosome exerts far tighter quality control than anyone ever suspected over its precious protein products… To their further surprise, the ribosome lets go of error-laden proteins 10,000 times faster than it would normally release error-free proteins, a rate of destruction that Green says is “shocking” and reveals just how much of a stickler the ribosome is about high-fidelity protein synthesis.

    So, somewhere on line there’s writing from Prof Shapiro (not sure if James or Robert) discussing the extreme fidelity of the copying process (assume that’s transcription/translation at genome site) [like 90+% accuracy]

    Behe uses these numbers in
    his Edge book

    does the quote above imply there’s quite possibly another layer of filtering at the genome, which would (apparently much) further improve the accuracy, by rejecting rna “inputs” that had copying errors at the earlier stage?

    or am I missing something?

    thanks

  53. BA77:

    sorry, that should say:

    another layer of filtering at the ribosome

  54. some text like this

    testing 123
    \

    more text like this

  55. es58, yes there is another level (multiple levels actually) of EXTREME error correction at the DNA/genome level:

    notes:

    Although evolution depends on ‘mutations/errors’ to DNA to make evolution plausible, there are multiple layers of error correction in the cell to protect against any “random changes” to DNA from happening in the first place:

    The Darwinism contradiction of repair systems
    Excerpt: The bottom line is that repair mechanisms are incompatible with Darwinism in principle. Since sophisticated repair mechanisms do exist in the cell after all, then the thing to discard in the dilemma to avoid the contradiction necessarily is the Darwinist dogma.
    http://www.uncommondescent.com.....r-systems/

    There are three major DNA repairing mechanisms: base excision, nucleotide excision and mismatch repair.
    http://www.web-books.com/MoBio/Free/Ch7G.htm

    Scientists Decipher Missing Piece Of First-responder DNA Repair Machine – Oct. 2009
    Excerpt: The first-responder machine, a protein complex called Mre11-Rad50-Nbs1 (or MRN for short), homes in on the gravest kind of breaks in which both strands of a DNA double helix are cut. It then stops the cell from dividing and launches an error-free DNA repair process called homologous recombination, which replaces defective genes.
    http://www.sciencedaily.com/re.....164106.htm

    Quantum Dots Spotlight DNA-Repair Proteins in Motion – March 2010
    Excerpt: “How this system works is an important unanswered question in this field,” he said. “It has to be able to identify very small mistakes in a 3-dimensional morass of gene strands. It’s akin to spotting potholes on every street all over the country and getting them fixed before the next rush hour.” Dr. Bennett Van Houten – of note: A bacterium has about 40 team members on its pothole crew. That allows its entire genome to be scanned for errors in 20 minutes, the typical doubling time.,, These smart machines can apparently also interact with other damage control teams if they cannot fix the problem on the spot.
    http://www.sciencedaily.com/re.....123522.htm

    Researchers discover how key enzyme repairs sun-damaged DNA – July 2010
    Excerpt: Ohio State University physicist and chemist Dongping Zhong and his colleagues describe how they were able to observe the enzyme, called photolyase, inject a single electron and proton into an injured strand of DNA. The two subatomic particles healed the damage in a few billionths of a second. “It sounds simple, but those two atomic particles actually initiated a very complex series of chemical reactions,” said Zhong,,, “It all happened very fast, and the timing had to be just right.”
    http://www.physorg.com/news199111045.html

    DNA ‘molecular scissors’ discovered – July 2010
    Excerpt: ‘ We discovered a new protein, FAN1, which is essential for the repair of DNA breaks and other types of DNA damage.
    http://www.physorg.com/news197902053.html

    More DNA Repair Wonders Found – October 2010
    Excerpt: This specialized enzyme may attract other repair enzymes to the site, and “speeds up the process by about 100 times.” The enzyme “uses several rod-like helical structures… to grab hold of DNA.”,,, On another DNA-repair front, today’s Nature described a “protein giant” named BRCA2 that is critically involved in DNA repair, specifically targeting the dangerous double-stranded breaks that can lead to serious health consequences
    http://www.creationsafaris.com.....#20101007a

  56. es58, perhaps someone else can offer better specifics on the fidelity of DNA replication, but as to what I have, Richard Dawkins stated in ‘The Blind Watchmaker’ page 123-124

    ‘How good would each typists have to be, in order to match the DNA’s performance? The answer is almost to ludicrous to express. For what it is worth, every typists would have to have an error rate of about one in a trillion; that is, he would have to be accurate enough to make only a single error in typing the Bible 250,000 times at a stretch. A good secretary in real life has an error rate of about one per page. This is about a billion times the error rate of the histone H4 gene. A line of real life secretaries (without a correcting reference) would degrade the text to 99 percent of its original by the 20th member of the line of 20 billion. By the 10,000 member of the line less than 1 percent would survive. The point near total degradation would be reached before 99.9995% of the typists had even seen it.
    http://books.google.com/books?.....38;f=false

  57. Hello again Andrew,

    You suggest that we should not be making an argument against the occurrence of beneficial mutations just because we haven’t observed them. I’m not sure anyone is (More like, can you get enough of them to generate all of the specified complexity required to transform a single-celled common ancestor into humans, flowers and whales. I imagine most people here agree with Behe’s “Edge of Evolution” for instance). That said, I would suggest that believing in something despite the absence of observational or experimental data is allowing evolutionists special knowledge (faith, if you like) that is simply not available to them from the scientific method. You don’t This is why it is also wrong for materialists to continue believing that life made itself because that conviction is appealing to non-scientific knowledge (ie. we’ve never observed life making itself and we can’t recreate the conditions for life making itself so believing it happened anyway is a matter of faith, not fact).

    The same reasoning applies to prokaryotic worms: what observation or experiment supports the belief that a prokaryote evolved into a eukaryote? And why did prokaryotes not become extinct while the eukaryotes thrived? And doesn’t this miss the point? We’re not trying to discover the origin of eukaryotic worms: we’re trying to work out why the only prokaryotic organisms that have ever existed are simply bacteria. Evolutionists might say maybe it’s because “multi-celled organisms require eukaryotic cells”. I would say, “you can’t have your cake and eat it”. They can’t have it both ways: they can’t argue that bacteria provides the best evidence for evolution when in fact they know full well that bacteria can never be anything other than bacteria. If that is the case, then prokaryotes cannot shed any light on how it is that a single eukaryote evolved into all other life on Earth. It also invalidates the use of computer simulations to inform us about evolution because they are all based on the premise that all life needs is replication, mutation and selection. It further invalidates the statements of evolutionist astronomers who argue that where the conditions of life arise, life too will arise and evolve because “multi-celled organisms require eukaryotic cells”.

    Bacteria don’t tell us that “multi-celled organisms require eukaryotic cells”. Bacteria tells us that life cannot evolve after all, for if bacteria can’t evolve into humans then nothing can.

  58. Sometimes things don’t change so fast:

    see here:

    http://mbe.oxfordjournals.org/...../1637.full

    While googling, I stumbled on a paper
    cited above by BA77:

    one more quote from there

    excerpt:

    does such a close relationship to modern bacteria mean that isolate 2-9-3 is itself modern? The answer to this question must be sought by resolving what appears to be an increasingly common paradox. We have a large set of rigorous geological and microbiological data which can be interpreted in favor of the antiquity of these organisms, and an equally large set of rigorously obtained molecular data which can be interpreted in favor of their modernity.

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