Home » Intelligent Design » Hybridization as a Challenge to Common Descent?

Hybridization as a Challenge to Common Descent?

Here’s an article from New Scientist that will be open for the next seven days to registered viewers. It’s about the “metamorphosis” of species from larval to adult stages, and brings in the views of Donald Williamson.

Here’s a link to his 2006 paper, and the entire abstract (it’s worth it!):

Examples of animal development that pose problems for Darwinian evolution by ‘descent with modification’ but are consistent with ‘larval transfer’ are discussed. Larval transfer claims that genes that prescribe larval forms originated in adults in other taxa, and have been transferred by hybridization. I now suggest that not only larvae but also components of animals have been transferred by hybridization. The ontogeny of some Cambrian metazoans without true larvae is discussed. The probable sequence of acquisition of larvae by hemichordates and echinoderms is presented. I contend (1) that there were no true larvae until after the establishment of classes in the respective phyla, (2) that early animals hybridized to produce chimeras of parts of dissimilar species, (3) that the Cambrian explosion resulted from many such hybridizations, and (4) that modern animal phyla and classes were produced by such early hybridizations, rather than by the gradual accumulation of specific differences.

Another day; another bad day for Darwinism!

  • Delicious
  • Facebook
  • Reddit
  • StumbleUpon
  • Twitter
  • RSS Feed

156 Responses to Hybridization as a Challenge to Common Descent?

  1. And an even worse day for the design argument as yet another non-teleological explanation for the complexity of life is proposed.

  2. Mark:

    Why non teleological? The classical problem of dFSCI, and the classical opposition between random non teleological mechanisms and directed mechanisms remain valid, whatever the proposed scenario.

    I declare that, whatever random mechanisms are proposed, the argument for design remains the same, and always valid. The only way to explain biological information by random systems is to prove that biological information is simple.

    Or to show that there are necessity mechanisms that favor functional complexity, other than (the inefficient :) ) natural selection. Are there? What are they?

  3. So, you now accept that the neo-darwinistic mechanism of natural selection acting upon random mutation is hopelessly inadequate in attempting to explain living organisms?

    We told you so, all along. What else are you wrong about and what else are we right about? Those are the questions you should now be asking.

  4. I am not qualified to judge the adequacy of natural selection acting on point mutations (which I guess is what you mean). I can only comment on the logic that says because there is evidence for an alternative mechanism for evolution which does not entail design therefore design!

  5. I declare that, whatever random mechanisms are proposed, the argument for design remains the same, and always valid. The only way to explain biological information by random systems is to prove that biological information is simple.

    Gpuccio – I am not sure what you mean by “random”? Do you mean “non-teleological”? If so your argument appears to be:

    “whatever non-teleological mechanisms are proposed, the argument for design remains the same, and always valid.”

    So how can ID be falsified?

  6. Sorry failed to close the quote properly.

  7. I was describing “the conventional view of evolution as a selection-biased random walk through the limitless space of possible DNA configurations” and, as an atheistic evolutionist, you must admit that, despite the fact you are “not qualified to judge”, you put a lot of faith in the explanatory power of this (now empirically falsified) evolutionary mechanism.

    Put whatever spin on it you like, Mark, but it’s definitely another bad day for Darwinism!

  8. Chris

    A “random walk through the limitless space of possible DNA configurations” suggest a fairly precise definition on the lines of

    * life is determined by the exact configuration of DNA in an organism,

    * all bases pairs have an equal and independent probability of changing into any other base pair at every instance of reproduction

    If you want to call this view Darwinism then that is your privelege. I challenge you to find any evolutionary biologist, past or present, who holds this view. The paper is not relevant to this idea, but as no one holds it that is hardly relevant.

    A more common interpretation of “random” variation is variation that is not directed towards any end. This is what virtually all biologists believe, might well be called Darwinism, and is quite compatible with Hybridization.

    However, the paper and the post was about descent with modification which is quite different.

    Really you guys need to grow out of counting every development in evolutionary biology as a blow against Darwinism and a blow for design.

  9. markf:

    Notice what I highlighted:

    that modern animal phyla and classes were produced by such early hybridizations, rather than by the gradual accumulation of specific differences.

    Williamson has an explanation for the Cambrian Explosion. Does neo-Darwinism. Does evo-devo?

    Hybridization happens at the chromosomal level; not the genetic, and not the amino acid level.

    You see no challenge to standard Darwinian theory in any of this?

  10. markf:

    You write:

    A “random walk through the limitless space of possible DNA configurations” suggest a fairly precise definition on the lines of

    * life is determined by the exact configuration of DNA in an organism,

    * all bases pairs have an equal and independent probability of changing into any other base pair at every instance of reproduction

    If you want to call this view Darwinism then that is your privelege. I challenge you to find any evolutionary biologist, past or present, who holds this view. The paper is not relevant to this idea, but as no one holds it that is hardly relevant.

    First:

    NO ONE, that is, NO ONE, believes that “life is determined by the exact configuration of DNA in an organism. So this is just fluff.

    Second:

    Your statement: “all bases pairs have an equal and independent probability of changing into any other base pair at every instance of reproduction” happens to be true. You should read Stephen Meyer’s The Signature in the Cell where he documents that this is true.

    So, when you say that I can’t “find any evolutionary biologists, past or present, who holds this view,” I suggest that this is the very problem we face.

    Donald Williamson held these views since the 50′s. And he was ignored for 50+ years by the Darwinian establishment because it challenged their orthodoxy. The problem ID faces is this very same Darwinian orthodoxy, of which, you seemed to have imbibed the “Kool-Aid”.

  11. Unlike ID, sciences that posit mechanisms require research to validate conjectures about the mechanisms. that could take decades or even centuries.

    If your mechanism is the assertion that some unspecified entity having unspecified capabilities did some unspecified things at unspecified time and places, then you are worry free.

    The argument isn’t even about which is right. It’s about what kind of conjectures suggest and inspire research.

    In the golden age when nearly all scientists were theists, they were either looking for evidence of a global flood (a mechanism for altering landscapes) or for understanding the divine clockwork. In both cases they were looking for regular behavior in the physical world.

  12. Pav

    NO ONE, that is, NO ONE, believes that “life is determined by the exact configuration of DNA in an organism. So this is just fluff.

    So we are agreed on that – great.

    Your statement: “all bases pairs have an equal and independent probability of changing into any other base pair at every instance of reproduction” happens to be true. You should read Stephen Meyer’s The Signature in the Cell where he documents that this is true.

    I have read The Signature in the Cell and can find no proof of that. It is clearly false that all base pairs have an independent probability of changing into any other base pair – just think about recombination, insertion, transposition.

  13. You see no challenge to standard Darwinian theory in any of this?

    Depends what you mean by standard Darwinian theory. Primarily this is a challenge to the standard account of the history of evolution. It is perfectly consistent with common descent, natural selection and current models of how genetic variation can happen (which have always included hybridization as a possibility). But most important from your point of view it is a non-teleological account of certain aspects of the history of evolution. So it provides no evidence of design whatsoever.

  14. Mark:

    No, I divided possible non design mechanisms into two components: RV and necessity mechanisms.

    For the RV part, I declared:

    “I declare that, whatever random mechanisms are proposed, the argument for design remains the same, and always valid. The only way to explain biological information by random systems is to prove that biological information is simple.”

    IOWs, complex functional information can never emerge from a purely random system (easily falsifiable, I believe).

    For the necessity part, I stated:

    “Or to show that there are necessity mechanisms that favor functional complexity, other than (the inefficient) natural selection. Are there? What are they?”

    IOWs, a purely random system cannot generate dFSCI. A purely random system + NS cannot do that. If you know other necessity mechanisms that can be coupled to a purely random system and behave better, please declare what they are.

    Design can generate dFSCI (very easy to demonstrate). Therefore, the design inference remains the best explanation for what is observed (dFSCI in biological beings) and cannot be explained in any other way.

    The design inference can easily be falsified in two different ways:

    a) Demonstrate that design cannot generate dFSCI (but we know that it can)

    b) Show that non design algorithms, including or not RV, can generate dFSCI. And, possibly, that those algorithms (which anyway don’t exist) can explain biological information better than design.

    So, the design inference is falsifiable. It will never be falsified, however, because it is true :) .

  15. Mark:

    I can only comment on the logic that says because there is evidence for an alternative mechanism for evolution which does not entail design therefore design!

    Well, I suppose your phrase was intended as “because there is no evidence”.

    Here, you fall again (although we have discussed the thing many times) in the false reasoning that ID is a logical deduction. You know well it is not so.

    ID is an empirical inference. You know very well the difference.

    So, the correct formulation is:

    “Because there is no credible explanation by an alternative mechanism for evolution which does not entail design, then design remains the best explanation”.

    And that is an absolutely correct statement, whether you believe it to be true or not.

  16. markf:

    It’s hard for me to reconcile your statement that you’ve read SITC and that there is no proof for this assertion. It forms a rather basic part of Meyer’s argument.

  17. Petrushka:

    Wow! What a negative view of ID!

    Let me ask you two questions:

    (1) The amount of genetic diversity in DNA was, based on Darwinian expectations (hence, of predictive value), thought to be low. But, when in the early 60′s, this premise was scientifically examined, huge amounts of variation was in fact found. Does this “falsify” Darwinism in any way?

    (2) Contrary to Darwinian thinking, those in the ID camp took the position that protein-coding genes in the genome of animals only represented a sort of “tool box” of materials to be used in constructing an organism, whereas, what truly defined an organism was a “blueprint”, EXPECTED by IDists, to be found in layers of logic/control/regulatory networks. Hence, Darwinists thought “junk DNA” to be no more than that, “junk”, whereas IDists were confident that some function, likely important, would be found for it. With the recent discovery of a regulatory function for putative “junk DNA” is the ID viewpoint validated?

    As to:

    It’s about what kind of conjectures suggest and inspire research.

    Had ID-thinking held sway, rather than Darwinism, cancer research would have taken a different, more productive direction a long time ago. And, “junk DNA” would have been investigated for possible function much sooner. So, is Darwinism a help, or a hindrance, to scientific inquiry. And, does ID put an end to scientific inquiry, or does it simply direct it along fewer, more productive lines?

  18. markf:

    What do you mean by hybridization? Can you spell it out?

  19. Had ID-thinking held sway, rather than Darwinism, cancer research would have taken a different, more productive direction a long time ago. And, “junk DNA” would have been investigated for possible function much sooner.

    You will no doubt be able to provide links to the writings of ID advocates that suggested lines of research supporting this claim. I mean writings made “a long time ago” with specific research proposals.

    The simple fact is that the discoveries you cite as evidence for the failings of mainstream science were made by mainstream science.

    And the more we know about cancer, the less likely it is that there will be a magic bullet. The very facts you cite make it highly unlikely that any single approach will be effective.

    So given all that, what lines of research are currently being proposed by Behe, Dembski, Axe, and Luskin? You seem to think ID has 20/20 hindsight. What about foresight?

    If you had a lab, what experiment would you run that isn’t already in the works?

  20. Gpuccio

    No. For once this was not a typo. I meant what I wrote:

    I can only comment on the logic that says because there is evidence for an alternative mechanism for evolution which does not entail design therefore design!

    Pav has put forward an alternative mechanism for evolution which does not entail design – hybridization – and seems to think this strengthens the case fof design.

  21. Hybridization is the combination of the genomes of two members of two different species to produce a hybrid which is different from both of them. Hybrids are not usually viable although sometimes they are and this might potentially be a way new species are created.

  22. Pav – you can easily solve this. Just indicate where he demonstrates that all base pairs have an independent probability of changing into any other base pair. I remember quite a lot of discussion for believing that base pairs have an equal probability of mutating into another base pair – nothing addressing independence – which is would be hard for him to do as it is quite clearly false.

  23. I’m sorry PaV but that’s a load of rubbish.


    Your statement: “all bases pairs have an equal and independent probability of changing into any other base pair at every instance of reproduction” happens to be true. You should read Stephen Meyer’s The Signature in the Cell where he documents that this is true.

    Really, Meyer disproved tranition bias? Or GC content? This sounds like a very important work!


    Donald Williamson held these views since the 50?s. And he was ignored for 50+ years by the Darwinian establishment because it challenged their orthodoxy. The problem ID faces is this very same Darwinian orthodoxy, of which, you seemed to have imbibed the “Kool-Aid”.

    No, Williamson is ignore becuase his ideas are insane. Holometabolous organisms don’t have two genomes, or evidence for past hybridisation. This is the guy who asked researchers to try mate a butterfly with a onychophoran!

    But I guess you are right that Williamson is ignored for similar reasons to ID…

  24. Morning Mark,

    I was quoting James A Shapiro, remember him? You were hoping that his new book “Evolution: A View from the 21st Century” would strike a killer blow against ID.

    If you’re right then Shapiro is wrong. You don’t honestly believe that do you? He is much higher up the food-chain than you are (and I know how much that means to evolutionists).

  25. Chris – when you say you were quoting Shapiro presumably you mean:

    “the conventional view of evolution as a selection-biased random walk through the limitless space of possible DNA configurations”

    I was trying to pin down what you meant by that. If it was a quote then perhaps you can explain what Shapiro meant by it (assuming you understood what he was saying).

  26. No problem, Mark. What he meant by it was that the conventional view of evolution is that it is a selection-biased random walk through the limitless space of possible DNA configurations.

    Anything else you need clearing up or do you now admit that Shapiro is right and you are wrong?

  27. Mark:

    I apologize, I had not understood what you meant.

    Anyway, I am happy I could restate an important general point :) .

  28. If Shapiro meant:

    all bases pairs have an equal and independent probability of changing into any other base pair at every instance of reproduction

    then clearly he made a mistake. I suspect he meant something different.

  29. GP:

    I only add, that the reason for that predictable impotence, is that search spaces grow exponentially with complexity. So, once something is narrowly specific — thus, it lives in isolated zones of interest aka islands of function — it will be maximally unlikely to be found by feasible scopes of search on the gamut of our solar system or observed cosmos.

    Digitally coded, functionally specific, complex information dFSCI in your abbreviation], credibly, is just such an islands of function phenomenon. That is, once we get beyond about 500 or 1,000 bits worth of such info, the resources of the solar system or even the observed cosmos as a whole, even if dedicated to the task of searching the config space in question, would sample so small a fraction of the possibilities, that we could only reasonably expect that configs that are typical would turn up.

    At 500 bits, if we were to use the 10^57 atoms of our solar system for its conventional lifespan of some 10^17 s, changing state every Planck time [the smallest time that makes physical sense] — it takes some 10^30 Planck times for the fastest chemical reactions — we could only sample 1 in 10^48 of the over 10^150 possibilities.

    Translating into more familiar terms, the equivalent challenge would, roughly, be: to try to find a needle in a cubical haystack a light month across, by taking a sample of the size of one straw. A solar system could be lurking in that haystack, but so long as the search is not intelligently directed on specific information, overwhelmingly, you would come up with what is typical — straw — not what is atypical. For very excellent sampling theory reasons. (And, strawmannising objectors, kindly note: this result is not dependent on any particular probability model or calculation; as you already know or should have known long before you made such objections in the first instance — i.e. the objections are plainly irresponsible and willfully misleading. The result is essentially the same as that on which for instance, pollsters trust samples of 1,000 or so to give good enough results on the US population at large.)

    The only serious non-intelligent guidance alternative on the scope of our observed cosmos is that life is somehow programmed into the chemistry and underlying physics of Carbon-based molecules in aqueous media.

    And if you were to demonstrate that, you would shoot your case in the head. For, that would demonstrate the ultimate form of cosmological front loading, and would immediately warrant an inference to design of the cosmos. Talk about Hoyle’s observation on monkeying with the physics of the cosmos!

    This is the context in which many have opened themselves up to the belief that we live in a quasi-infinite multiverse.

    But, that, too, is no escape:

    1 –> This is philosophical, metaphysical speculation, not science; as the required basis of observations is simply not there.

    2 –> And, if you have changed the subject to philosophy, ALL serious worldview options sit to the table of comparative difficulties as of right, not sufferance of the materialist magisterium in the holy lab coat. (In short, no materialist a prioris, please; especially when smuggled in through question-begging methodological assumptions and historically unjustified assertions and caricatures of, say ethical theists of the ilk of a Copernicus, a Galileo, a Newton, or a Kelvin or in our day a Schaeffer or a Sanford.)

    3 –> The relevant cosmological evidence cumulatively — i.e this is a rope not a chain argument; you would have to cut across the cluster of fibres — strongly points to our observed cosmos sitting at a finely tuned operating point that, if tipped slightly in any one of dozens of ways, would lead to our cosmos being radically unsuited to the sort of C-chemistry cell based life we observe and experience.

    4 –> Even through multiverse scenarios, that raises the issue of the bullet that swats the locally isolated fly on the wall, and/or the need for a cosmic bread factory set up to bake up sub-cosmi that closely explore the neighbourhood of the physics of our observed cosmos. That is, the multiverse speculation simply promotes the fine-tuning, complex functional programming/organisation of the physics of the cosmos issue up to the next level; it does not remove it.

    5 –> So, even through a multiverse speculation, we are back to the issue that the best explanation for what we see in our world, and especially in the code-based heart of biological life, is design.

    6 –> And, once we see that for biological life we have to account for 100,000 to 1 mn bits or so of functionally specific digital information, then we will see that for major body plans, we need to account for 10 – 100 mn bits, dozens of times over. (E.g. I was just looking at a description of how plants make wood fibres and bind them together — an amazing nanofactory!)

    [ . . . ]

  30. 7 –> The dFSCI search space challenge applies to not only origin of life, but its elaboration into major body plans. And, again, the only empirically warranted source for dFSCI is design; which is backed up by the needle in haystack and monkeys at keyboards type analyses and simulations that objectors are so desperate to deflect.

    8 –> All you would have to do to irretrievably break design theory, would be to credibly empirically demonstrate how by chance and mechanical necessity, without intelligent intervention, dFSCI can originate on a reasonable scope of resources.

    (If there was such in hand, there would be no need for the sort of nasty, false accusation, caricature based personal attack — and, “here he is and here his family is shooters, go git em . . .” outing tactics — laced rhetoric that we so often see from objectors to design theory, and as I have again been subjected to by yet another wave of attacks at Anti Evo; attacks that reveal the underlying supercilious contempt, hostility and perhaps hate that seems to drive too many of the objectors to design thought. That this is the level of objections we so continually meet, is absolutely revealing on the balance of the case on the merits, and on the balance on moral credibility and basic broughtupcy too. And, AE denizens, before you play the your’e a hater who hit back first or the you’re [im]morally equivalent false accusations games, kindly check here [notice, I am dealing with a destructive constitution law imposition!] and here (go to the onward links) and address these responsibly; reflecting that on this sort of topic, I am doing investigative analysis and then writing empirically backed up — factually anchored — exposes. SHAME ON YOU!)

    9 –> Wikipedia, testifying against interests, tells us about the monkeys at keyboards challenge:

    The [infinite monkeys] theorem concerns a thought experiment which cannot be fully carried out in practice, since it is predicted to require prohibitive amounts of time and resources. Nonetheless, it has inspired efforts in finite random text generation.

    One computer program run by Dan Oliver of Scottsdale, Arizona, according to an article in The New Yorker, came up with a result on August 4, 2004: After the group had worked for 42,162,500,000 billion billion monkey-years, one of the “monkeys” typed, “VALENTINE. Cease toIdor:eFLP0FRjWK78aXzVOwm)-‘;8.t” The first 19 letters of this sequence can be found in “The Two Gentlemen of Verona”. Other teams have reproduced 18 characters from “Timon of Athens”, 17 from “Troilus and Cressida”, and 16 from “Richard II”.[21]

    A website entitled The Monkey Shakespeare Simulator, launched on July 1, 2003, contained a Java applet that simulates a large population of monkeys typing randomly, with the stated intention of seeing how long it takes the virtual monkeys to produce a complete Shakespearean play from beginning to end. For example, it produced this partial line from Henry IV, Part 2, reporting that it took “2,737,850 million billion billion billion monkey-years” to reach 24 matching characters:

    RUMOUR. Open your ears; 9r”5j5&?OWTY Z0d…

    10 –> That is, searches of spaces of order 10^50 are feasible, but that is well short of searching spaces of order 10^150 or 10^300, which would require 72 – 143 ASCII characters, not 20 – 24 or so. (We will leave off for the moment the further challenges to find where such a success has happened and then put it to work in a functional system!)

    11 –> In short, there is abundant and excellent reason to accept the judgement of common sense: the best explanation of dFSCI such as posts in this thread, is intelligence. And, here is no credible alternative to intelligence, so when we see dFSCI in the heart of life, it strongly points to such life being the product of design. Life gives the appearance of design, and that is best analytically explained as being due to the credible conclusion that it is in actuality designed.
    __________

    Onlookers, that is the context for GP’s remarks in conclusion just above:

    Design can generate dFSCI (very easy to demonstrate). Therefore, the design inference remains the best explanation for what is observed (dFSCI in biological beings) and cannot be explained in any other way.

    The design inference can easily be falsified in two different ways:

    a) Demonstrate that design cannot generate dFSCI (but we know that it can)

    b) Show that non design algorithms, including or not RV, can generate dFSCI. And, possibly, that those algorithms (which anyway don’t exist) can explain biological information better than design.

    So, the design inference is falsifiable. It will never be falsified, however, because it is true :) .

    GEM of TKI

  31. I think Shapiro was perfectly clear, he was merely describing neo-darwinism or the belief in the explanatory power of natural selection acting upon random mutations. I know this. Deep down, you know this too. But, as per usual, you refuse to admit you’re wrong. You’d rather suggest that Shapiro, someone who is certainly more qualified than you (and I know how much that means to evolutionists) “made a mistake” instead.

    It’s exchanges like this which demonstrate the fact that evolutionists will resort to intellectual dishonesty rather than admitting they were wrong. Especially when they have to admit it to ID proponents!

    So, let us be quite clear here. The neo-darwinistic mechanism of natural selection acting upon random mutation is hopelessly inadequate in attempting to explain living organisms. This is why the likes of Donald Williamson and James Shapiro feel the need to propose completely different mechanisms.

    Hybridization or Lamarckism may turn out to have an empirical basis after all. Then again, they may not. But, what is indisputably clear – right now – is the fact that a mechanism requiring natural selection acting upon random mutations is hopelessly inadequate and so must be abandoned by any truth-seeker.

    Are you a truth-seeker, Mark? If so, then you must agree with me and James Shapiro. Any other response simply confirms that you (like most of the other atheistic evolutionists here) put your strong atheistic commitments before reason and evidence.

  32. markf:

    I investigated the possibility with a colleague of mine named Tony Mega, an organic chemist. I asked him if there were any physical or chemical differences between the bases or attachment sites on DNA that could account for base sequencing. We considered this question together for a while, but soon realized that there are no significant differential affinities between any of the four bases and the binding sites along the sugar-phosphate backbone. Instead, the same type of chemical bond (an N-glycosidic bond) occurs between the base and the backbone regardless of which base attaches. All four bases are acceptable; none is chemically favored.

    This meant there was nothing about either the backbone of the molecule or the way any of the four bases attached to it that made any sequence more likely to form than another. Later I found that the noted origin-of-life biochemist Bernd-Olaf Kuppers had concluded much the same thing. As he explained, “The properties of nucleic acids indicate that all the combinatorially possible nucleotide patterns of a DNA are, from a chemical point of view, equivalent.” In sum, two features of DNA ensure that “self-organizing” bonding affinities cannot explain the specific arrangement of nucleotide bases in the molecule: (1) there are no bonds between bases along the information-bearing axis of the molecule and (2) there are no differential affinities between the backbone and the specific bases that could account for variations in sequence.

    One nucleotide base is completely interchangeable with another. Since there is no chemical determination, then the nucleotide sequence represents a true code.

  33. Pav

    I thought you might mean that bit. It is one reason for supposing that all base pairs are equally likely to mutate into any other base pair.

    1) It does not address the influence of factors external to the DNA string. For example, does being on the end of a chromosome make a base pair more likely to mutate? I have no idea – but it is the kind of thing that would affect this probability. wd400 sounds like someone who actually knows what they are talking about.

    2) It does nothing to show that the probabilities are independent and a even moment’s consideration shows they are not. Point mutations, maybe, but all other kinds of mutations affect strings of base pairs.

  34. wd400:

    Really, Meyer disproved tranition bias? Or GC content? This sounds like a very important work!

    No, what Meyer demonstrated was the independence of individual bases along any length of DNA. This is pertinent due to the implication that no natural bias exists in the formation of the genetic code. This is part of the initial “random walk through the limitless space of possible DNA configurations” that “origin of life” researchers must contend with.

    Now, if neo-Darwinists want to point to some kind of “transition bias”, any such bias represents but an inconsequential diminishing of an otherwise astronomically large configuration space.

    Further, this is from a 2003 paper:

    Our analyses show that genes and regions with widely varying base composition exhibit uniformity of transition mutation rate both within and among mammalian lineages, as long as the transitional mutations caused by CpG hypermutability are excluded. The estimates show no relationship to potential intrachromosomal or interchromosomal effects. This uniformity points to similarity in point mutation processes in genomic regions with substantially different GC-content biases.

    As to GC-content, I don’t see the pertinence of this whatsoever. Who knows what function it plays in DNA. If “life” has a preference for such “content”, so what? Is this preference somehow anticipated by what we know of biochemistry? I think not.

  35. markf:

    It does nothing to show that the probabilities are independent and a even moment’s consideration shows they are not. Point mutations, maybe, but all other kinds of mutations affect strings of base pairs.

    First, you might want to look at the quote I included in my answer to wd400.

    Second, mutations do, indeed, affect strings of base pairs. But the Darwinian hypothesis is that these are “random” changes. So isn’t your argument that there is a non-randomness involved?

    The ID argument is that the space of protein-coding DNA is utterly too large to have any kind of random beginning.

    This should just be obvious to anyone who investigates microbiology.

  36. Chris

    I am a truth seeker. No doubt you are too. Please lay off the abuse.

    I believe that your case is based on not exploring in detail what is meant by:


    neo-darwinistic mechanism of natural selection acting upon random mutation

    Williamson’s hypothesis (which is far from proven) is inconsistent with some aspects of evolutionary theory but not others. I am trying to explore which ones. You seem totally uninterested in doing this and when I try to pin you down you quote Shapiro. As I do not have his book this is of little use to me – so ask you what Shapiro meant. (I did not say he made a mistake. I said if he meant what I conjecture you mean then he would be wrong, but I also said I doubted he meant that).

    In response you revert to the mantra “The neo-darwinistic mechanism of natural selection acting upon random mutation” and then call my attempts at getting some clarity intellectual dishonesty.

  37. markf:

    Pav has put forward an alternative mechanism for evolution which does not entail design – hybridization – and seems to think this strengthens the case fof design.

    Mark, hybridization, described by Williamson, undermines the case for Darwinism. Why? Because there is no such thing as “common descent”, the hinge-pin of Darwin’s theory.

    Additionally, each of these “hybrids” have to have some kind of origin? Well, what is it? If there is no such thing as common descent, then how did diverse forms arise? The logical inference is that some kind of intelligent agency is at work. Thus the design inference is strengthened, not weakened.

  38. Pav – like Chris you are playing games with the different possible meanings of “random”.

    (A) No respectable biologist would propose that genetic variation is random in the sense of all base pairs having an equal and independent probability of mutation.

    (B) However, almost all biologists would say the variation is mostly (with the exception of some evidence of Larmarckism) not directed towards any end and in particular it is not directed towards increasing the fitness of the organism.

    Hybridization, which takes place all the time, is a classic and well known example of variation which is not random in sense (A) but is random in sense (B). All that Williamson seems to be claiming is that hybridization once took place across whole phyla. It would appear from WD400 that this is not taken seriously by the biological community, but even if it were it would not be in conflict with (B).

  39. Sorry Mark, but I think everybody here understands exactly what is meant by the “neo-darwinistic mechanism of natural selection acting upon random mutation”. How much more clarity do we need? And if it is a mantra, that is only because neo-darwinists constantly rely upon it to explain the amazing things we see in nature.

    What we have here is a moment where the likes of Williamson and Shapiro are saying that there is a major problem with that mantra and there is a need for evolutionists like you to explain exactly where you now stand. Do you still accept neo-darwinism or do you (like Williamson and Shapiro) now reject neo-darwinism. I do not feel like your responses have been straight or unambiguous in this regard, hence the charge of intellectual dishonesty. It is not personal abuse, it is simply an observation of the position you have adopted on this thread so far.

    Let’s be straight with each other and we’ll have no problem.

  40. Chris – if you understand exactly what is meant by the “neo-darwinistic mechanism of natural selection acting upon random mutation” then it should be trivial for you to explain what “random mutation” means. I have given two alternative definitions in 2.1.2.2.6 above. Can you say which one you mean or is it neither of these? It should take you no more than three or four words to answer this.

  41. Mark (et al):

    I would like to briefly comment on your definitions in 2.1.2.2.6:

    No respectable biologist would propose that genetic variation is random in the sense of all base pairs having an equal and independent probability of mutation.

    I think you certainly understand the point, but still I would like to specify, for tyhe benefit of all, that the fact that events have the same probability of happening is in no way a requisite of a random system. That is a property of a very special probability distribution, the uniform distribution. So, even if genetic variation were made of events having different probabilities, it could well be a completely random system. The only part of the darwinian algorithm that is not random is NS, that is the expansion of those random events that confer a reproductiove advantage.

    That said, I agree with you that the probability of events in RV at the biological level is not necessarily completely uniform. First of all, if we are talking the transition from one protein to a new, unrelated one, variations near the original protein are certainly more likely, given that the most common tool of variation is probably point mutation. That’s why we describe genetic transitions as a “random walk”, which is not exactly like tossing a coin, even if the probabilistic consequences are not so different.

    That said, I believe however that a uniform distribution for nucletides (and therefore for aminoacids) is still the best approximation of the system for big transitions, because nucleotides (and aminoaxcids) have really a rather independent chance of being reprersented in the random variation events, even taking into account some asimmetries. Even events like inversion, hybridization and similar, which are more “macroscopic” than point mutations, in the end cannot create real differences, if we consider that any random inversion, or hybridization, is in principle possible. Applying combinatorics may not be easy, but I think it can be done.

    Obviosuly, there can be some biochemical necessity mechanisms that can alter the simmetries and make the distribution somewhat non uniform (but random all the same), but that’s where your second point is pertinent.

    However, almost all biologists would say the variation is mostly (with the exception of some evidence of Larmarckism) not directed towards any end and in particular it is not directed towards increasing the fitness of the organism.

    That’s the really important point. Whatever the probability distribution, or even the contribution of some necessity aspects from biochemical laws (except for NS), the point is that none of that can possibly favor the kind of functional information we observe in proteins, because neither RV nor biochemical laws have any pertinent information about the sequence of functional proteins.

    The first point is rather obvious, unless someone thinks that empirical probability distributions exist that include information about functional protein sequences.

    The second, if it were not true, would be a strange and strong argument in favor of theological evolutionists, and I believe that neither you nor I are on that side.

    So, to sum up:

    a) RV is always random, whatever the form or the probability distribution. It can in no way overcome the “probability barrier” of a random walk towards functional complexity. It doesn’t matter if the variation mechanism is point mutation, inversion, duplication, hybridization, or whatever. The system remains random. The results remain random.

    b) The only non random mechanism in darwinian theory (and, I believe, in any non design theory) is NS. I will not repeat here the arguments against its “creative” powers. The only point I want to make here is: NS is not random, it is a necessity principle, and it is the only pertinent necessity principle that can change something (but not much) in an explanation of protein information. But, as all necesiity mechanisms, it must be explicitly understood, and its real import must be explicitly evaluated, before it can be accepted as relevant to an explanation.

  42. And you accuse me of playing games, Mark! Fine, I’ll play along with yours:

    Random = without method or conscious decision (ie. accidental, not designed)
    Mutation = an alteration or change

    So a random mutation is an alteration or change that is made without method or conscious decision (i.e. an accidental, not designed alteration or change).

    You give me the impression that you want to redefine “random mutation” so that it doesn’t mean the above. Is this because you are worried that neo-darwinism has been found out (and found seriously lacking) by 21st century science?

  43. But Pav, hybridization is consistent with common descent. It happens all the time and biologists do not find it in anyway inconsistent with evolutionary theory. All that Williamson is proposing is that hybridization occurred between wildly different species and this played a large role in the creation of new phyla. If true, this would pose problems for the tree of life model i.e. descent with modification – but it is not a problem for the idea that all life is descended from a small number (possibly one) common life form. As such it is an alternative non-teleological explanation for the diversity of life.

  44. Chris – I don’t want to define random in any way. I just want to know how you define it. We seem to have settled on something like my definition B above. This is fine. Must biologists believe this to be true. Nothing that Williamson proposes conflicts with this view of random mutation. Hybridization takes place without method of conscious decision. I have not read Shapiro but I am willing to bet that nothing he proposes conflicts with it either.

  45. Mark,

    Don’t persuade yourself that Williamson and Shapiro’s views can be reconciled with a belief that natural selection acting upon random mutations can explain how man evolved from microbes. If that we true, then we wouldn’t be discussing either of them.

    The indisputable fact is, both of them realise the hopeless inadequacy of neo-darwinistic mechanisms and so propose entirely different mechanisms that have nothing to do with natural selection acting upon random mutations.

    So, the question that you have still not answered is, do you agree that neo-darwinism has failed or do you still want to place your faith in it? If the former, then we told you so. If the latter, then how do you explain your fundamental difference of opinion with Williamson and Shapiro (who are certainly not neo-darwinists)?

  46. BTW, I am clicking on the ‘Reply’ button but the post isn’t being nested in the conversation (I’m currently using Safari on Mac OS X 10.7.1)

  47. Chris – you have an odd way of arguing which seems to consist of repeating your assertion more stridently without any supporting facts or arguments.

    I do believe that that Williamson views can be reconciled with a belief that life evolved through natural selection acting upon random mutations (in the sense of “random” which I hope we have now agreed). I bet this is also true of Shapiro from the summaries I have seen – but I have not read his work in detail. You don’t agree (except you seem so confused it is hard to be sure). That is why we are discussing them.

    Now, unlike you, I will present an argument rather than just assert that everyone here knows I am right and it is intellectually dishonest of you to disagree.

    Hybridization occurs all the time. It is just the mixing of genomes from two different species. It does not conform to any method and is not the result of any conscious decision. So it is random in the sense we defined above.

    Williamson is proposing is that new phyla were formed through hybridization between very different species. This process is still lacking in method and is not the result of a conscious decision. Therefore the resulting variation is random in the sense we defined. The result is still subject to natural selection and might thrive or fail.

    What makes you so certain Williamson and Shapiro are not neo-Darwinists? There are certainly aspects of current evolutionary theory they dispute but there is nothing in their work that I can see that conflicts with random mutation and natural selection as the driving force behind evolution.

  48. The only reason I repeat my argument, Mark, is because you cannot or will not address my argument. That is as true of this subject as it was true of atheistic morality. You seem to think that as long as you say something, (anything, no matter how irrelevant!) or appeal to authority or argue ad hominem that that constitutes a rebuttal to an argument.

    Well, guess what? It doesn’t. So, until you admit you are mistaken, or make your excuses and leave, then it is only right that I continue to make the argument, perhaps pose it in slightly different wording until you finally get it. Because I’m not the one who is confused here.

    No supporting facts or arguments? You haven’t even demonstrated an awareness of what it is I am arguing in the first place, let alone refuted it. So, for your benefit only (as the record clearly demonstrates where I’m coming from and your rather evasive responses so far):

    1. The OP – Williamson turns to hybridisation because a neo-darwinistic mechanism cannot explain the Cambrian Explosion.

    2. James Shapiro has written a book (that you haven’t even read, but still want to argue about) that is quite clearly about over-turning the old neo-darwinistic belief in “the conventional view of evolution as a selection-biased random walk through the limitless space of possible DNA configurations”.

    These two points, which I’ve made already more than substantiate my argument that neo-darwinism is in serious trouble. Let me now add that Shapiro even goes further by embracing the “informatic perspective” of “systems engineering” and the genome as a “read-write storage system”, rather than a read-only storage system. How can that be reconciled with your belief that microbes evolved into man through natural selection acting upon random mutations? How many more times will you simply pretend that this question has not been asked?

  49. Chris Doyle, please refer to the full sentence from Shapiro’s introduction to his new book on evolution:

    “Thinking about genomes from an informatic perspective, it is apparent that systems engineering is a better metaphor for the evolutionary process than the conventional view of evolution as a selection-biased random walk through the limitless space of possible DNA configurations.”

    I’ve highlighted the word “metaphor” to make the point that Shapiro was suggesting a possibly more fruitful way of thinking about evolutionary history. He was not questioning the fact of evolution or the naturalistic basis of life’s diversification through time.

  50. 1. The OP – Williamson turns to hybridisation because a neo-darwinistic mechanism cannot explain the Cambrian Explosion

    That is your opinion as you have asserted in many different ways – but not even attempted to prove. How can I address the argument when you haven’t made one in the first place? I can address your assertion. I have said I think it is false and explained why. I will try again.

    My position is that Williamson’s position is consistent with neo-Darwinism.

    I have argued for this by first agreeing what we mean by neo-darwinism, most importantly what is meant by random mutation, then tried to demonstrate that Williamson’s position is compatible with this by pointing out that hybridization is just a form of random mutation.

    As you say I have not read Shapiro’s book which is why I am trying to stick to the issue in the OP.

  51. As to Williamson’s work, do you have a neo-Darwinian explanation for the Cambrian Explosion?

    Now, don’t try the easy way out and say, “Oh, it wasn’t an explosion. There was plenty of time. Etc, etc.” Because Darwinians have done studies trying to disprove the explosive nature of the Cambrian and have had to conclude that it was, indeed, and ‘explosion’.

    To try and deny the Cambrian Explosion, or to otherwise use neo-Darwinism as an explanation is not, well, ‘insane’; but it is highly irrational, I’m afraid.

  52. As I do not have his book this is of little use to me – so ask you what Shapiro meant.

    I have the Shapiro book, and what he means is that there are many kinds of genomic change that are much more potent than point mutations. Many, such as duplication and transposition, provide opportunities for large scale prototypical changes.

    He also has a rather aggressive view of evolvability, and asserts that organisms can initiate genomic changes in response to environmental stress. He likened the process to what happens in the immune system.

    He does not say the changes anticipate specific need, only that by increasing the rate of change, the probability of successful adaptation is increased. Actually, he explicitly denies that that future need can be anticipated.

    If there’s any doubt about my interpretation, take a look at the first Shapiro thread, where I posted extensive quotes. I can provide more selections if anyone thinks I quote mined.

  53. If by “engineering,” you mean a system like the immune system that responds to environmental triggers by increasing the quantity of genomic changes, that would be Sahpiro’s metaphor.

    Shapiro’s evolution is entirely mechanistic and entirely without foresight. He just think’s it is really effective. More so than a view that claims all change is tiny.

  54. Petrushka,

    For goodness sake, please re-read the book (if you have actually read it in the first place) because there is no way you can say that “Shapiro’s evolution is entirely mechanistic”. Did you miss this bit, right at the front of the book?

    The contemporary concept of life forms as self-modifying beings coincides with the shift in biology from a mechanistic to informatics view of living organisms. One of the great scientific ironies of the last century is the fact that molecular biology, which its pioneers expected to provide a firm chemical and physical basis for understanding life, instead uncovered powerful sensory and communication networks essential to all vital processes, such as metabolism, growth, the cell cycle, cellular differentiation, and multicellular morphogenesis. Whenever these processes have been subjected to the most advanced types of biological analysis, the number of regulatory interactions and control molecules inevitably has grown to rival (and frequently out- number) the molecules dedicated to executing the basic biochemical and biomechanical events [30]. Paralleling the contemporaneous transformation from a largely mechanical-industrial society to a densely interconnected information-driven society, the life sciences have converged with other disciplines to focus on questions of acquiring, processing, and transmitting information to ensure the correct operation of complex vital systems.

    The take home point from Shapiro is not what he’s proposing to account for evolution but the fact that he’s rejecting neo-darwinism.

  55. Daniel King, you’re missing the point. I didn’t say Shapiro doesn’t believe in evolution. I said that he rejects a neo-darwinistic explanation for it. Don’t you think that is significant, given that evolutionists have been trying to defend neo-darwinism in the face of an irresistible ID onslaught?

    Did you read Chapter Two of his book, where he says:

    A little thought will make it clear how difficult it is to maintain the traditional idea that each individual component of these elaborate circuits evolves by making its own independent random walk through the enormous space of genome sequence possibilities.

    Nothing remotely metaphorical about that, Daniel, you must agree.

  56. So now you’re asking me to prove that hybridisation is not the same as natural selection acting upon random mutations? Unbelievable. It’s not that you cannot understand the point here, but rather that you refuse to accept it.

    Williamson felt that natural selection acting upon random mutations could not account for the Cambrian explosion. He is not alone in that sentiment. Therefore he proposed a completely different mechanism… and was heavily criticised for this heresy by his evolutionist colleagues (I don’t buy Williamson’s alternative either by the way).

    But it is not the fact that he proposes hybridisation that you should be concerned about. It is the fact that he rejects natural selection acting upon random mutations… that mechanism is hopelessly inadequate. He knows it. Shapiro knows it. Most of the people here know it. You do too, deep down, but you choose to live in denial. Funny how we’ve reached the same conclusion as we did regarding atheistic morality – moral atheists must live a lie rather than admit the truth.

    If you really can’t tell the difference between copying errors and hybridisation then you really are wasting time here.

  57. So now you’re asking me to prove that hybridisation is not the same as natural selection acting upon random mutations? Unbelievable.

    To be precise I asking you to prove that hybridisation is not a type of random mutation using the definition of “random” we agreed. I have argued that it conforms to that definition – (there is no method or decision behind it) and also pointed out that hybridisation happens all the time and is not regarded as being in any kind of conflict with standard evolutionary theory. Your argument is to write “unbelievable”.

    One reason for your confusion may be that in your last sentence you appear to identify random mutation with copying errors. They are a kind of random mutation but not the only kind. For example, recombination following sexual reproduction is also random mutation but it is not a copying error.

  58. So Mark, when evolutionists talk about natural selection acting upon random mutations, they’re not really talking about random mutations taking place in DNA as a result of copying errors. That’s only a tiny insignificant part of the story, right? In fact, hybridisation is what you had in mind all along (not that there’s any real difference in your eyes) yes?

    And I suppose that you also believe that you can get a flying pig when you breed a pig with a pigeon.

    “Unbelievable” is a true and fitting response to your intellectually dishonest position.

  59. markf:

    To be precise I asking you to prove that hybridisation is not a type of random mutation using the definition of “random” we agreed. I have argued that it conforms to that definition – (there is no method or decision behind it) and also pointed out that hybridisation happens all the time and is not regarded as being in any kind of conflict with standard evolutionary theory.

    There’s a big distinction between the kind of “hybridization” we’re familiar with and that of which Williamson is speaking of in his theory.

    Modern-day hybridization involve, generally, species-to-species crosses, or genus-to-species crosses.

    Williamson is talking about crosses between individuals at the “class” level of phylogeny. Very different.

  60. Chris, I’ve learned the hard way that you need to go to the nearest “reply” above which you want to post. IOW, there could be a post with the “reply” option showing; and then two or three posts with no such “reply” option showing. To respond to one of the two or three following the last “reply” option showing, click that “reply” and then post.

  61. KF

    With regard to your expanded discussion above on The dFSCI search space challenge, the depth of thought (and understanding) of this challenge by a typical materialist scientist is on display in the Oct issue of New Scientist.

    When discussing how proteins might have evolved to include structures that exploit quantum physics phenomena, the response was:

    [he] shrugs his shoulders…”Life’s 4 billion years of nanoscale R&D will have engineered many miracles,” he says. We should learn to accept what we see and try to mimic it.

    Needless to say, no follow-up question was asked as to how an unforesighted process could develop a framework to innovate with nanoscale machinary let alone discover quantum-mechanical sensors.

  62. So Mark, when evolutionists talk about natural selection acting upon random mutations, they’re not really talking about random mutations taking place in DNA as a result of copying errors. That’s only a tiny insignificant part of the story, right?

    Chris – sarcasm and accusations of dishonesty do not prove anything. I never claimed that copying errors were insignificant – only that there are other types of random mutation and hybridisation is one of them. Did you do GCSE biology and get a reasonable grade? If so, you should know that copying errors are one type of random mutation. Others include recombination during sexual reproduction – by far the biggest source of mutation in sexually reproducing species. Hybridisation is, of course, a subset of sexual reproduction.

    If Gpuccio is reading this perhaps he would be good enough to explain as you are more likely to read and learn from him.

  63. Pav

    There’s a big distinction between the kind of “hybridization” we’re familiar with and that of which Williamson is speaking of in his theory.

    Modern-day hybridization involve, generally, species-to-species crosses, or genus-to-species crosses.

    Williamson is talking about crosses between individuals at the “class” level of phylogeny. Very different.

    Yes they are different in scale. But you need to explain why one is a counter-example to modern evolutionary theory and the other is not.

  64. Patronised by someone who can’t tell the difference between a flying pig and a copying error! Fantastic!

    At least answer me this, Mark: where exactly did the body plans come from before their hybrids accounted for the Cambrian explosion: natural selection acting upon random mutations or not?

  65. Still maintaining the verbal abuse Chris! And still not a single argument to support the statement that Williamson is incompatible with neo-Darwinism. Not a single one after so many requests – just verbal abuse and sarcasm. It is becoming obvious that you don’t have an argument.

    where exactly did the body plans come from before their hybrids accounted for the Cambrian explosion: natural selection acting upon random mutations or not?

    I don’t actually think that Williamson’s hypothesis sounds very plausible. I am just pointing out that if it were true that it would be consistent with random mutation plus natural selection. I do believe that the body plans around at that time were the result of random mutation and natural selection. But that is changing the subject and I don’t plan to embark on that well worn theme.

    Anyway I need to go to bed and I am unlikely to have any more time to waste on this next week.

  66. Chris Doyle:

    Daniel King, you’re missing the point. I didn’t say Shapiro doesn’t believe in evolution. I said that he rejects a neo-darwinistic explanation for it. Don’t you think that is significant, given that evolutionists have been trying to defend neo-darwinism in the face of an irresistible ID onslaught?

    I think I took your point, but my point is that Shapiro’s theory is a naturalistic theory. As such, it may represent an amendment, an addition, or even a complete replacement of neo-darwinism. If it is fruitful, it will be a paradigm shift that will stimulate future research in biology. And scientists will be grateful.
    But that is no help to ID, which so far has shown scant interest in experimental science.

    Did you read Chapter Two of his book, where he says:

    A little thought will make it clear how difficult it is to maintain the traditional idea that each individual component of these elaborate circuits evolves by making its own independent random walk through the enormous space of genome sequence possibilities.

    Again, you quote out of context. See the following sentence:

    As you will see, there are alternative ways, based on established molecular processes, to think about the efficient evolution of genomic circuits based on rapid distribution of transcriptional regulatory sequence motifs.

    (My emphasis)

  67. KF, from your post:

    Functionally specific, complex information and associated information [FSCO/I] — especially, digitally coded FSCI [dFSCI] — are seen as two of the strongest signs of design as cause.

    You signify design as “cause”. I thought an intelligent/intentional agent was a “cause”, not design. Design is interpreted as a signifier for a particular type of cause, isnt it?

  68. It really is very simple, Mark. Crossing a pig with a pigeon is not a neo-darwinistic mechanism. You are trying to blur a very clear distinction (between hybridisation and copying errors) for the sole reason that you cannot or will not face up to the fact that the likes of Williamson and Shapiro are abandoning neo-darwinism. Thanks to your atheist convictions, you prefer spin to truth.

    Sometimes I find it hard to resist giving as good as I get. What I’ve been getting from you today has been very disappointing, especially considering your age and qualifications. Your behaviour certainly undermines all of the claims that you made on your blog many months ago. Maybe you just had a bad day (hard as that is to believe in this lovely weather we’ve been having!) I hope the next time we cross paths you’ll produce the reasonable opposition I’ve come to expect from you. Until then, all the best.

  69. PaV et al.

    This whole discussion is bizarre.

    (1) Williamson is crazy, there is no reason for a ‘Darwinist’ or anyone else to take him seriously.

    (2) You doing very strange things to Shaprio’s quoute.

    Seems to me, that he is trying to say that modern evoluoinary biology is a very narrow sort of darwinian theory (much more narrow, than, for instance, Darwin’s) that equates genotype with destiny and thinks, for instance, there are no constraints of mutation.

    Of course, Shapiro is erecting a strawman there. No one in their right minds thinks there are no constraints of mutations – tranistion bias being the obvious example. So evolutionary biologists know those things exist, they just aren’t sold they they add up to much.

    But what no one has been able to say is why their presence of a particular constraint on mutation would make a blind bit of difference for the plausibility evolutionary biology?

  70. Morning Daniel,

    I don’t think you do “take my point” otherwise you wouldn’t think I was quoting out of context. You seem to think the context is evolution in general or even methodological naturalism. It is neither. The specific context is the central neo-darwinistic mechanism of natural selection acting upon random mutations.

    It is frankly irrelevant to my argument to consider the completely different alternative evolutionary mechanisms that Williamson and Shapiro propose. The only thing that matters is neo-darwinism and its doctrine about the creative power of natural selection acting upon random mutations. And the fact that Williamson and Shapiro have rejected neo-darwinism.

    Look at the bold parts in the quote provided in the OP. Look at my two Shapiro quotes. They all converge on the same very important truth: neo-darwinism is wrong. Can you not appreciate the enormity of that admission?

    You say “Shapiro’s theory…may represent…a complete replacement of neo-darwinism” then follow that up with “And scientists will be grateful.” Ha! I’m sure plenty of scientists will be queuing up to admit that they wasted their entire careers trying to find evidence for neo-darwinism. I can just see Richard Dawkins in a press conference now: “Sorry folks, every word I’ve ever written was complete and utter nonsense!”

    ID proponents have been criticising neo-darwinism for a long time now and many have suffered professionally as a result of it. Most are ridiculed by their evolutionist colleagues. And yet, if neo-darwinism turns out to be false (as Shapiro and Williamson seem to believe) then that is revolutionary stuff, don’t you agree?

    Before you get all excited about the replacement theories offered by the likes of Shapiro and Williamson, you would do well to digest the fact that more and more neo-darwinists are coming out and admitting that natural selection acting upon random mutations is a hopelessly inadequate mechanism to account for life. Do not underestimate the significance of that admission.

  71. Hi wd400,

    It’s funny that Williamson has come up in discussion here because he cropped up in another discussion I was having elsewhere a couple of weeks ago. Only this time, it was an evolutionist proposing that “Darwin’s Dilemma” has been solved by Williamson!

    Do you have any links or sources that support your claim that “Williamson is crazy, there is no reason for a ‘Darwinist’ or anyone else to take him seriously”? Not because I disagree with you (though I think you’re treatment of Williamson is harsh, after all, he is just being honest and saying neo-darwinism cannot explain the Cambrian explosion) but because I’d like to see for myself what others in the scientific community have been saying about him.

  72. It is frankly irrelevant to my argument to consider the completely different alternative evolutionary mechanisms that Williamson and Shapiro propose. The only thing that matters is neo-darwinism and its doctrine about the creative power of natural selection acting upon random mutations. And the fact that Williamson and Shapiro have rejected neo-darwinism.

    Chris, you and Williamson and Shapiro are entitled to your opinions. Whether it will make any difference to science only time will tell.

    Look at the bold parts in the quote provided in the OP. Look at my two Shapiro quotes. They all converge on the same very important truth: neo-darwinism is wrong. Can you not appreciate the enormity of that admission?

    The bolded hypotheses expressed by Williams will have to be tested. Time will tell.

    I can just see Richard Dawkins in a press conference now: “Sorry folks, every word I’ve ever written was complete and utter nonsense!”

    Can you see Isaac Newton, having been corrected by Einstein, saying the same? Science is a process, not a destination.

  73. SteveO

    It apparently has not occurred to these folks to do the sort of calculation that, say, Abel did, on the Planck Time Quantum State [PTQS] resources of our solar system [or our Planet for that matter or even the observable cosmos].

    Somewhere in a decent course on computer science, you will learn that trial and error is not good enough as a search, beyond a very limited context. As, you run out of adequate resources real fast.

    Here is my summary “needle in a haystack” explanation — in response to the usual strawmannish rhetoric out there in the Darwinista fever swamps [they have totally lost any sense of proportion or decency] — of why FSCI beyond 500 – 1,000 bits just simply is not a reasonable result of blind chance and mechanical necessity.

    Solar system level:

    Chi_500 = I*S – 500, bits beyond the solar system threshold

    If this metric goes positive and you are operating on the solar system scale, as macroevo would — OOL would be on the cosmological scale [go up to 1,000 bits!] — you are entitled to infer design as best causal explanation. The solar system PTQS resources would go through about 10^102 states in 10^17 s [~ solar system lifespan to date on the conventional timeline]. That is 1 in 10^48 of the set of possibilities for 500 bits. Or, roughly a single straw-sized sample from a cubical haystack, a light month across.

    Basic sampling theory tells us that overwhelmingly, such a sample will pick up what is typical, not what is utterly atypical, and that would obtain even if a whole solar system were lurking in the bale.

    No need for specific probability models and the usual side-tracking debates on such.

    The answer is blatantly obvious; save to those ideologically indoctrinated in a priori materialism (often disguised by question-beggingly redefining science materialistically), committed and polarised to the point of closed mindedness.

    That is why I no longer think the issue is whether we can SHOW the reasonableness of inferring design by mere cogency of argument, to the satisfaction of those we are dealing with. Cogent evidence that is compelling has long been on the table, but it is not being accepted because it cuts across a priori commitments.

    Stronger medicine is needed: the mind-bending games being played by the materialist ideologues in lab coats have to be exposed, until they have been broken to finally feel ashamed to make their claims in public.

    When that finally happens, then maybe the case can be heard on the merits. We need to present the case, indeed, but right now the issue is that the mind-bending games must be exposed.

    Not to mention, the bully-boy Saul Alinsky thuggish tactics.

    (And, when you guys decided to try to hold my family hostage, you crossed a nuclear threshold. I can have no respect for those who behave like that, and no decent person should have any respect for such. Senseless, ruthless, heartless, shameless, utterly depraved; even, reprobate. BYDAND!)

    So, we should not be surprised to see some to the trade rags of the evo mat magisterium and their popularisers sticking to the patently absurd and pretending or even imagining that the obviously absurd makes good sense: 2 + 2 = 5, or the like.

    Nihilists like that will only stop when they can no longer get away with what they are doing. That is in effect what Plato implied in his expose of evo mat, in The Laws BK X 360 BC, 2350 years ago.

    GEM of TKI

  74. Chris, and this is not a loaded question: can you tell me what you understand by the phrase “selection-biased random walk through the limitless space of possible DNA configurations”?

    The reason being that mutations are only “random” in the sense that they are only predictable in a probabilistic sense. They are not random in the sense of “equiprobable” because all mutations have actual causes, and the sum of those causes does not produce a flat probability distribution of changes.

    For example SNPs (single nucleotide substitutions) are only one kind of mutation – Copy Number Variants (CNVs) are also extremely common, and important, and this means that sequences that already exist, and code for either a protein or some regulatory function are much more likely to reappear than a sequence de novo.

    So it’s important to understand what “random walk” really is. A “random walk” is different from a “random draw”. The analogy is usually that of a drunkard who starts at a certain lamp post, and takes a step either up or down the street with equal probability. But that means that any new step will not land him with equal probability anywhere in the street. Every new step will land him with certainty very close to where he already is, the only uncertainty being whether it will be slightly further north or slightly further south.

    If we have a whole gang of drunks staggering up and down the street, and then blow a gentle breeze in one direction, so that the drunks who are facing the breeze at any given time are slightly refreshed and those who aren’t, slightly more likely to collapse into a stupor, then that would be analogous to natural selection – you will end up with more drunks at the end of the street from which the breeze is blowing than at the other end.

    What Shapiro is saying, as I understand him, is that there is more to it than this – that the actually probability of stepping up or down is itself constrained, that the net bias does not merely result from natural selection, but from a bias that affects the drunk’s probability of stepping north versus south.

    That mutations that have a chance of selective success have rather higher probability of occurring than you’d expect if the mutation process itself had not been subject to some kind of selection process.

    Which of course is perfectly consistent with Darwin’s theory, but very interesting – it simply adds a higher order – that evolvability itself evolves. Which you can demonstrate fairly readily in computer simulations, if you allow heritable variance in the probability not only with which offspring will survive, but in the probability with they will resemble their parents.

  75. Chris, I have to say that I do NOT know “what is meant” by “neo-darwinistic mechanism of natural selection acting upon random mutation”.

    Specifically, I do not know what you mean by this phrase. If we are to communicate clearly across what is quite a wide gulf, it is important to be very specific, I think.

    And the word “random” is used in a great many senses, and what the phrase means depends crucially on what the writer intends to denote by the word “random”.

  76. OK, if by “random” you mean “without method or conscious decision” then I’d like to know what you mean by “method” because all mutations have a cause and many are produced by well-understood mechanisms (methods?), e.g. duplication, deletion, and recombination.

    Moreover it is not a definition that any mathematician would recognise! Mutations occur by means of stochastic processes, in other words, they are only statistically predictable, and are drawn from a probability distribution. But that probability distribution need not be flat, and, indeed, most naturally occurring probability distributions are far from flat.

    Shapiro’s point is the the probability distribution itself is shaped by evolutionary processes.

    I’d also add that conscious decisions are also probabilistic! You can consciously decide not to decide – or to “toss a coin”. There is some evidence that we may actually do this internally, on occasions, as a defense strategy, to avoid being “second guessed” by an enemy.

  77. P:

    Are you serious?

    From they days of Plato in The Laws, Bk X, it has been immemorial, that we can analyse causal factors and processes in terms of chance and/or necessity and/or ART or design.

    That tweredun inferred on reliable empirical signs, is plainly distinct from Whodunit.

    Design as process evident from empirically reliable signs, is not to be confused with designers who are for good reason habitually associated with designs. We may reliably know the one without having good reason to infer to a particular agent as designer, as those who conclude murder or arson by persons unknown will tell you.

    But of course, all of this is in a rhetorical context.

    So, let me put the matter plainly: from the very first ID technical work, TMLO by Thaxton et al in 1984, it was explicitly understood and stated that while there is good reason to at least consider and even infer to design as cause from signs in life forms, this alone does not then immediately warrant a direct conclusion to the specific identity or ontological nature of the designer of the sort of cell based life we observe here on earth, whether within or beyond the cosmos. As I have frequently said here at UD, a molecular nanotech lab some generations beyond Venter et al — who have provided undeniable proof of concept — could do it.

    So, the likes of Barbara Forrest et al are indulging in willful, agenda- serving and insistent- in- the- teeth- of- repeated- correction misrepresentation of design theory.

    LYING, in one word.

    Lying that has done harm, and for which one day such will have to give a very serious accounting.

    Now, there is, of course, another level of design theory that DOES raise some very interesting issues that point to a designer beyond our cosmos, cosmological design. For just one instance, lifelong agnostic astrophysicist and Nobel Equivalent prize holder, the late Sir Fred Hoyle, is on record:

    From 1953 onward, Willy Fowler and I have always been intrigued by the remarkable relation of the 7.65 MeV energy level in the nucleus of 12 C to the 7.12 MeV level in 16 O. If you wanted to produce carbon and oxygen in roughly equal quantities by stellar nucleosynthesis, these are the two levels you would have to fix, and your fixing would have to be just where these levels are actually found to be. Another put-up job? . . . I am inclined to think so. A common sense interpretation of the facts suggests that a super intellect has “monkeyed” with the physics as well as the chemistry and biology, and there are no blind forces worth speaking about in nature. [F. Hoyle, Annual Review of Astronomy and Astrophysics, 20 (1982): 16.]

    I do not believe that any physicist who examined the evidence could fail to draw the inference that the laws of nuclear physics have been deliberately designed with regard to the consequences they produce within stars. [["The Universe: Past and Present Reflections." Engineering and Science, November, 1981. pp. 8–12]

    H, He, C, O and N are the five most abundant elements in the observed cosmos, are key building-block elements of life, and their abundance is locked into the physics of the cosmos. The above and many other considerations lead many cosmologists to conclude that our observed cosmos sits at a very fine tuned operating point that facilitates the existence of C-chemistry aqueous medium cell based life.

    That strongly points to design of the observed cosmos — even through multiverse speculations [read the just linked] — and design targetted on life like we experience and observe. An extra-cosmic architect and builder of our cosmos, with knowledge, skill and awesome power, having intent to create life, is a very plausible and even compelling candidate for best explanation. And that has long been the case; Plato in fact makes just such a cosmological inference to best explanation in the Laws Bk X, and Newton follows suit.

    Such an architect and builder of our world, is then a very plausible candidate to be designer of our world of life. And in that context — pace the fulminations of Sagan, Lewontin, Coyne and co — ethical theism is as valid a framework for doing serious science as any other.

    But, you will look long and hard before you will find the likes of Forrest addressing that with any seriousness or fair-mindedness.

    Sorry, the plain evidence is that science in our day is being held hostage to ideological, a priori, intellectually bankrupt and morally bankrupt a priori evolutionary materialism imposed by a new magisterium dressed in the holy lab coat.

    It is time for the bankrupt reigning orthodoxy to be exposed.

  78. F/N: He of course is not a chemical foundation for life, it is a nuclear physics foundation for life.

  79. From they days of Plato in The Laws, Bk X, it has been immemorial, that we can analyse causal factors and processes in terms of chance and/or necessity and/or ART or design.

    And it is precisely that categorical division that is now at issue.

  80. Before you get all excited about the replacement theories offered by the likes of Shapiro and Williamson, you would do well to digest the fact that more and more neo-darwinists are coming out and admitting that natural selection acting upon random mutations is a hopelessly inadequate mechanism to account for life. Do not underestimate the significance of that admission.

    But they aren’t, Chris!

    You’ve created a straw man and called it “neo-Darwinism”. I think the problem is with the word “random”. It does not mean what you think it means :)

  81. OK, if by “random” you mean “without method or conscious decision” then I’d like to know what you mean by “method” because all mutations have a cause and many are produced by well-understood mechanisms (methods?), e.g. duplication, deletion, and recombination.

    Except they are not well understood as no one knows why these mutations occur.

    Mutations occur by means of stochastic processes,

    That’s the claim yet there isn’t any evidence to support it.

    Ya see ID says that mutations occur by means of internal programming.

  82. The heck with hybridization, sexual reproduction poses a problem for universal common descent.

    Ya see, with sexual reproduction, any one parent’s contribution to the gene pool can be eliminated in two generations! That is because only 1/2 of a parent’s genome is passed down (at a time). And that also means that even the most beneficial mutation can be lost in just one generation.

    Then there is sexual selection which also helps keep the norm.

    But anyway universal common descent is severly challenged for the simple reason that it cannot be objectively/ scientifically tested.

  83. Well Elizabeth, perhaps YOU can post what biologists mean when they say the mutations are random.

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

    I say they use the word to mean “entirely by chance; just happened for no purpose” IOW they use it just as dictionies define it.

  84. Greetings Lizzie,

    Your quarrel is with James Shapiro and co (as well as me!) I refer you to an online article from the FT press which contains a good excerpt from Shapiro’s “Evolution: A View From The 21st Century”.

    http://www.ftpress.com/article.....?p=1720625

    Do you think Shapiro has created a straw man of neo-darwinism too?

  85. Information processing is mechanistic, unless you are proposing that computers ore cells are non-material.

  86. So, you’re saying Shapiro is wrong to describe “the shift in biology from a mechanistic to informatics view of living organisms”, Petrushka? Do you deny that such a shift has occurred?

  87. Yes, I do, Chris, to some extent. I think he’s cariacaturing a position that nobody holds, just as Gould did.

    But what he is introducing, as I said, is interesting, which is the “evolution of evolvability”. It’s not a refutation, but an addition.

    Or it’s only a “refutation” of a straw man understanding of the word “random”.

  88. Do you think Shapiro has created a straw man of neo-darwinism too?

    To some extent I think he has.

    He is not really arguing against current mainstream biology. he is arguing against trying to stuff what biologists know into a 1940 paradigm that was focused on point mutations.

    Both Shapiro and Koonin seem to be saying there are much more powerful kinds of changes in genomes than base pair mutations. It’s not that genomic mutations are unknown or under-studied, but that they have not been properly incorporated into a definition of evolution.

  89. Wow, really? Why do you suppose a neo-darwinist would feel the need to create a straw man of neo-darwinism? It just doesn’t make sense.

    Unless of course, Shapiro is no longer a neo-darwinist. That fact alone is very significant don’t you think? Given his belief in evolution (and, presumably methodological naturalism) why would he turn from the sacred doctrine? Perhaps it’s because the evidence against neo-darwinism is so overwhelming… just like ID proponents have been saying from the beginning!

  90. All these claims of “strawman” yet not one offers up anything to support the claim.

    Typical of evolutionists…

  91. Elizabeth,

    “Evolution of evolvability. It’s not a refutation, but an addition.”

    Oh, boy! Poor Darwin. I mean poor chap. He couldn’t have guessed that his ideas would be taken to such an absurdity. This is getting really crazy, don’t you think?

    “Random” does not mean “random”? That is bizarre. I mean it really is. I think I am now positively losing the ability to parse it.

  92. Did you see gpuccio’s entry at 10:
    http://www.uncommondescent.com.....ent-401444

    I think he provides a very good summary of the ‘random’ part of “random mutations”.

    I find all this equivocation over neo-darwinism rather puzzling. It is apparently so true and easy to understand that we should be teaching it to primary school kids! I tell you, show me 100 evolutionists and I’ll show you 100 different set of ideas about what evolution really means.

  93. Yep, so it turns out that Lamarckism is the new Darwinism… wait a minute, wasn’t Darwin a Lamarckist?

  94. Random in biology means “not planned/ just happened for no purpose”

  95. Newton wasn’t corrected. Just extended to cases not available to Newton.

    There are degrees of being wrong. It’s about successive approximations. Newton still works perfectly for the range of velocities studied by Newton.

    Darwin’s formulation is still a good working approximation, but we now have a lot more detail. What’s amazing about Darwin is how many unsolved problems he recognized and wrote about. I see them continually brought up as if biologists had never considered them.

    The Cambrian, for example.

  96. Newton wasn’t corrected. Just extended to cases not available to Newton.

    Never tangle with a Newtonist. They are so defensive.

  97. Colleagues,

    Given that so many evidence based objections to the theory of evolution turn out to be actually its valuable additions and not refutations, is it possible to suggest at least anything that would be falsification enough for the TOE?

  98. Yep, so it turns out that Lamarckism is the new Darwinism… wait a minute, wasn’t Darwin a Lamarckist?

    Well, no, Lamarckism isn’t “the new Darwinism”. And yes, Darwin did consider it possible that variance was generated by Lamarck’s proposed mechanism (inasmuch as it was a mechanism – it was more a postulate). Lamarck wasn’t right, but he wasn’t completely wrong either. There are mechanisms by which the behaviour in one generation affects what the next inherits, one being via natural selection (the behaviour of other members of the population forms part of the environment to which subsequent generations adapt), the other being epigenetics, although that doesn’t produce mutations.

  99. Colleagues,

    Given that so many evidence based objections to the theory of evolution turn out to be actually its valuable additions and not refutations, is it possible to suggest at least anything that would be falsification enough for the TOE?

    Well, it depends what you mean by “the TOE”. If you mean the principle that populations adapt by means of heritable variance in reproductive success, possibly not, as it’s virtually a syllogism – i.e. is self-evidently true. You could falsify its application to biology by showing either that reproductive success is not heritable, but we know that it is!

    If you mean something else – perhaps that all heritable traits are genetic, then yes, that’s falisfiable, and has been falsified. It isn’t true.

    Possibly you meant neither of these things – if so, what do you mean by “the ToE”? In other words, what claim is it that you think should be falsifiable but may not be?

  100. Well Elizabeth, perhaps YOU can post what biologists mean when they say the mutations are random.

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

    I say they use the word to mean “entirely by chance; just happened for no purpose” IOW they use it just as dictionies define it.

    Well, “entirely by chance” doesn’t really help you – it just passes the buck to the word “chance”. If you mean “happened for no purpose” then that probably is what biologists mean, but “happened for no purpose” isn’t the same as “happened for no reason” or “was not caused by anything”.

    There are several causes of mutations, and while biologists would argue that they “happen for no purpose” (i.e. no-one intended them to happen) they certainly don’t “happen for no reason”, and what Shapiro and Margulis argue, persuasively, is that the reason that organisms mutate in the way that they do is that optimal mutation types and frequences are themselves selected at population level. Just as heritable variance in reproductive success at the level of the individual organism results in adaptation of the population, so heritable variance in adaptive success at the population level results in adaptation at the population-of-populations level.

    As I said, this is readily demonstrable by computer modelling.

  101. I don’t you know what you mean by “all this equivocation over neo-Darwinism” – it’s precisely to avoid equivocation that I want you to say exactly what you mean by the term!

    But Darwin’s basic principle that heritable variance in reproductive success leads to adaptation is certainly simple enough to be taught to primary school kids. Indeed, sunflower growing competitions are a great way to illustrate the point!

    Also, so is the principle of common descent, and can be readily illustrated. Most primary kids are delighted to recognise bird skeletons as miniature T Rex fossils, and to point out to less-well-informed adults that dinosaurs aren’t actually extinct.

    And I don’t actually agree with gpuccio’s post, though s/he makes some good points.

    I’ll comment there, though :)

  102. Hi, gpuccio!

    A few comments, as Chris Doyle pointed me to your post:

    I think you certainly understand the point, but still I would like to specify, for tyhe benefit of all, that the fact that events have the same probability of happening is in no way a requisite of a random system. That is a property of a very special probability distribution, the uniform distribution. So, even if genetic variation were made of events having different probabilities, it could well be a completely random system.

    Hmmm. You are of course right that “random” events need not have a uniform probability distribution, and most don’t (the direction of Brownian motion being a nice example of one that does!)

    But I still think the term “random” is misleading, because it has so many meanings in common English. If something has a 999/1000 probability of happening, you don’t usually call the result “random”, and “certainty” is approached asymptotically! For that reason I think “stochastic” is a better term, and then we are not tempted to apply the meaning “not on purpose”. We can intend events that are nonetheless stochastic. Drawing a bingo number is a deliberate act, done “on purpose” but it makes use of a stochastic process. So I think it’s really important to tease apart the concept of something being been drawn from a probability distribution from the concept of something being done on purpose.

    The only part of the darwinian algorithm that is not random is NS, that is the expansion of those random events that confer a reproductiove advantage.

    I disagree. Natural selection is just as much a stochastic process as mutation. However, it refers to a systematic bias in the direction of reproductive success.

    Mutations are not biased in the same sense (but then the concepts are not analogous either), although they are much more likely to have no effect on the reproductive success of de novo beaerr than to be deleterious or advantageous. So they are “biased” in favour of neutrality.

    But I’d say it is better to describe both systems as simply stochastic, where mutation has probability distribution with a peak around neutral, and breeding successfully has a probability distribution with a peak around mutations that confer some survival advantage to the phenotype in the current environment.

    That said, I agree with you that the probability of events in RV at the biological level is not necessarily completely uniform. First of all, if we are talking the transition from one protein to a new, unrelated one, variations near the original protein are certainly more likely, given that the most common tool of variation is probably point mutation.

    I think duplication and insertion, and, in the case of sexually reproducing species, recombination within an existing gene, are probably more common.

    That’s why we describe genetic transitions as a “random walk”, which is not exactly like tossing a coin, even if the probabilistic consequences are not so different.

    That said, I believe however that a uniform distribution for nucletides (and therefore for aminoacids) is still the best approximation of the system for big transitions, because nucleotides (and aminoaxcids) have really a rather independent chance of being reprersented in the random variation events, even taking into account some asimmetries.

    I don’t see how this belief is justified at all! In fact, I don’t even find it coherent. Are you suggesting that “big transitions” (not even sure what you mean by this – all transitions are achieved by means of incremental genotypic changes, even if occasionally, the phenotypic change may be fairly substantial) involve some kind of radical shuffling of the genome? If not, what do you mean?

    Even events like inversion, hybridization and similar, which are more “macroscopic” than point mutations, in the end cannot create real differences, if we consider that any random inversion, or hybridization, is in principle possible. Applying combinatorics may not be easy, but I think it can be done.

    Well, “hybridization”, which is simply mating between individuals with markedly different genomes, as opposed to mating between individuals with much more similar genomes, as generally happens, just means that radically novel alleles are more likely to arise by recombination. But as radical novelty in sequences is much more likely to be disastrous than slight novelty, I doubt it plays much role in adaptation.

    Obviosuly, there can be some biochemical necessity mechanisms that can alter the simmetries and make the distribution somewhat non uniform (but random all the same), but that’s where your second point is pertinent.

    However, almost all biologists would say the variation is mostly (with the exception of some evidence of Larmarckism) not directed towards any end and in particular it is not directed towards increasing the fitness of the organism.

    Well, epigenetic variation probably serves an important function, possibly at population-selection level. But epigenetic changes don’t alter the genome.

    That’s the really important point. Whatever the probability distribution, or even the contribution of some necessity aspects from biochemical laws (except for NS), the point is that none of that can possibly favor the kind of functional information we observe in proteins, because neither RV nor biochemical laws have any pertinent information about the sequence of functional proteins.

    What do you mean by this? In what sense could “RV” have “information”? What has “information” is the genome itself, and that information is the information laid down over generations as to what leads to survival in each environment through which the population has persisted.

    And every “RV” is a “probe” if you like, into the current environment, to “see” if there is anything that might come in useful, or even do no current harm, but might come in handy later.

    And yes, I’m using anthropomorphic metaphors, but then so are you :)

    So, to sum up:

    a) RV is always random, whatever the form or the probability distribution. It can in no way overcome the “probability barrier” of a random walk towards functional complexity. It doesn’t matter if the variation mechanism is point mutation, inversion, duplication, hybridization, or whatever. The system remains random. The results remain random.

    But it isn’t a random walk! You are forgetting that there is not one “walker” but millions, and only those that randomly take a step in a useful direction get to make the next step!

    “RV” is simply that – random variation. It doesn’t “walk” anywhere. What “walks” are the RVs that prove to be neutral, advantageous, or only slightly deleterious. So the “walk” is not “random” in your sense at all (though it is stochastic) but that is because the “walk” is the natural selection part, not the variation part!

    b) The only non random mechanism in darwinian theory (and, I believe, in any non design theory) is NS. I will not repeat here the arguments against its “creative” powers. The only point I want to make here is: NS is not random, it is a necessity principle, and it is the only pertinent necessity principle that can change something (but not much) in an explanation of protein information. But, as all necesiity mechanisms, it must be explicitly understood, and its real import must be explicitly evaluated, before it can be accepted as relevant to an explanation.

    I think you have some good points, but they are awfully muddled!

    “NS” isn’t really a process at all, it’s simply a consequence of heritable variation in reproductive success. That heritable variation is, indeed “random” with respect to reproductive success, in that a de novo mutation that is confers increased reproductive success in the current environment is no more probable, and indeed less – than one that is neutral or slightly deleterious.

    However because the vast majority of de novo mutations make virtually no difference to reproductive success in the current environment, they drift through the population by means of what you could legitimately call a “random walk”. However, to the extent that some variants do turn out, at some point, to confer reproductive advantage, that “walk” is biased in favour of those variants that happen to confer advantage in the current environment, and it is those variants that then stand a greater chance than the others of being the ones in whom the next potentially de novo mutation happens.

  103. Actually, Joseph, the parent’s contribution can be eliminated in one generation. It is an average of 1/2 the genes that are passed on. It is possible (although extraordinarily improbable) that none of one parent’s genes are passed on. The chances of none of a parent’s genes making it through two generations are also incredibly small – although slightly larger.

    However, none of this is relevant because the majority of both parent’s genes will be the same and will be part of common gene pool belonging to the species.

  104. Elizabeth,

    What I find disconcerting is that nobody seems to know what on earth the TOE should really exactly mean. That is a very bad sign suggesting that perhaps the whole concept is fuzzy and untenable. Many a biologist tacitly admit this, in the presence of strong evidence of its implausibility.

    I don’t know what you, Elizabeth, mean by the TOE, but I mean exactly what Darwin did as per the “Origin of Species”. I am quite ignorant as to the latest “additions and not refutations” as regards the theory, as you put it. As a layman in biology, I can only say that there are very few people who are willing to fight to the end at the side of the classical Darwinism (or neo-Darwinism). Perhaps, now it’s only Dawkins.

    What I find unhealthy about the contemporary variant of the TOE is that no matter what evidence against it is produced, this evidence gets built into the theory. As a result the “unshakable” theory gets another crutch and on it stumbles.

  105. Joseph,
    We could use the computer code methphor, if I know that some notable atheists share among each other, notably, that their father died before the horse. There is nothing exciting to do with it? I was, as you think chemistry knows, whither it is taking place in a movie Woody Allen complained about the alphabet and, most importantly, about information semantics, i.e. what is the best explanation?

    And that calculation is only for one single gene could do so much. Oops!

    It turns out that neither Darwin nor subsequent biologists have ever assumed that point mutations has been known since before 1950 and has been rigidly looked at, and a chemical soup with zero functional bits – zero to 130 bits and you must explain how it happens.

    “Intelligent” selection monitors on or two dimensions. Why should biology be an exception?

    Formally, for information, very good paper by Abel which explains very well the concept of targets and goals, you would like to point out that neither Darwin nor subsequent biologists have ever assumed that point mutations are neutral or neutral alleles.

    I find most interesting about autistic savants, is the same: spontaneous generation of information not only does one have to sneer at everything?

    As for me, for a minimal replicator of 130 bits and you must show that it puts the cart before the genes were knocked out! In fact at one time in one word.

  106. Well, UD seems to have spammed my reply. But to find what people think of Williamson read Hart and Grosberg (2009) PNAS who use the phrase “astonishing and unfounded”. Or Giribert (2009) in the same journal who went with “Why did the author ignore the weight of phylogenetic evidence that utterly falsifies his claim?”.

    On blogs you’ll fine “worst paper of the year” and a “preposterous hypothesis”

  107. Well…. you comment is utterly informed. No one calims common descent = every indidual in a population contributing to future generations so why would anyone bother with your odd claim?

    If you mean weakly benifical mutations are unlikely to be fixed well… that’s call the nearly neutral theory and it’s been around for more than 30 years.

    What amazes me is how little of evolution those that oppose the theory have bothered to learn.

  108. Dr Liddle:

    Kindly show us a process that has a beginning and cannot be described as one or more of these factors in action, i.e. it traces to a fourth factor, or else to no causal factor [including no necessary factors; cf here].

    Failing a credible empirical counter example, we are simply dealing with selectively hyperskeptical verbal objections unconnected to empirical reality.

    GEM of TKI

  109. PS: Dr Liddle, please do the half-burned match exercise and discuss your proposals in its light. Note especially the point that a necessary causal factor is a causal factor.

  110. Nothing has a single causal factor, kf, and causes can usually be considered on many levels, proximal and distal.

    Some events have proximal intentional causes, some distal intentional causes.

    Some events do not have intentional causes at all. And intentions fall on an continuum. Does a plant that moves a stone as it grows intend to do so? Does a worm? Or an ant? Or a person?

    As I see it, “intention” involves the creation of a forward model, the output of which is fed back into the decision-making process as input.

    Humans do this. Worms possibly do, at a very crude level. Plants probably don’t.

  111. “PS: Dr Liddle, please do the half-burned match exercise and discuss your proposals in its light. Note especially the point that a necessary causal factor is a causal factor.”

    My match burned my fingers when I turned it upside down.

    What lesson was I supposed to learn?

  112. Irrelevant.

    If you are objecting to analysing causal factors as mechanical necessity and/or chance and/or art, then show either things that begin to exist with NO — including no logically necessary causal factors — causal factors, or a fourth factor.

    Otherwise, you are simply making a verbal objection to be selectively hyperskeptical.

    I have said nothing against causal factors for a given outcome not being composite, just that — per massive experience — they will be analysable on chance and/or mechanical necessity and/or art. In that analysis, I further hold that we can often isolate factors responsible for aspects of many phenomena based on tested, reliable signs.

    let us know how the match exercise turns out.

    GEM of TKI

  113. What is the half-burned match exercise?

  114. Well, I’d argue that “chance” and “necessity” (which I don’t think are separate, in fact) underlie “art”, and what is necessary (but not sufficient) for “art” is feedback between output and input.

  115. Assertion, not evidence.

    And, not of causeless beginnings, nor of a fourth causal factor, but of ART being reducible to chance plus necessity.

    Kindly demonstrate it, empirically; without imposing materialistic a prioris that end up begging the question.

    And, along the way, please show that key empirical signs of design acting by art, are empirically shown to originate from chance plus necessity.

    Otherwise, we are simply looking at question-begging materialist a prioris censoring thought. As happened so blatantly with Lewontin, Sagan, Coyne et al.

  116. You did not follow basic instructions, to tilt it up so it would try to burn the already burned wood. Yet another distraction.

  117. Kindly cf here.

  118. points 10 – 13 ff

  119. Kindly note, tilt the head up . . .

  120. Excuse me, but how is it possible for none of one parent’s genes to get passed on?

    Has that ever been documented in humans?

  121. Nice non-response- I never claimed that common descent = every indidual in a population contributing to future generations- never.

    If you mean weakly benifical mutations are unlikely to be fixed well… that’s call the nearly neutral theory and it’s been around for more than 30 years.

    Even very beneficial mutations are unlikely to be fixed.

    What amazes me is how little of evolution those that oppose the theory have bothered to learn.

    Nice unsupported nonsense…

  122. Ok.

    Imagine a population of 10 000 fixed for an allele we’ll call “-”. A new mutation pops up making the allele “+”, and the finesses are

    “-/-” : 0.98
    “+/-” : 0.99
    “+/+” : 1.0

    That’s hardly “very beneficial”. Given that you think beneficial mutations can’t be fixed I guess you think there is no chance that “+” will be in this scenario?

    (and if you don’t think common descent predicts everyone in a population contributes tot he next generation, then I really can’t understand you point about recombination)

  123. Imagine a population of 10 000 fixed for an allele we’ll call “-”.

    Exactly- your position relies on imagination not science.

    Given that you think beneficial mutations can’t be fixed…

    I didn’t say nor think that. I said:

    Even very beneficial mutations are unlikely to be fixed.

    Sexual reproduction sees to that.

    So you seem to have issues with reading what I post. Oh well.

    (and if you don’t think common descent predicts everyone in a population contributes tot he next generation, then I really can’t understand you point about recombination)

    What point was that?

  124. Even very beneficial mutations are unlikely to be fixed.

    So, how likely is that the mutation I talked about, that gives the tiny rise in fitness I talked about, gets fixed? What do you think? 1%? 0.1%?

  125. What point was that?

    What ever point you were trying to make. As I say, I don’t understand it, so it’s really up to you to make it.

  126. 1- “Beneficial” is a relative word meaning what is beneficial for one generation in one specific environment isn’t necessarily going to be beneficial for the next generation in a slightly different environemnt.

    2- Competing “beneficial” mutations- your scenario doesn’t account for them. I guess that is why it is imaginary.

    3- Your scenario also doesn’t account for sexual reproduction

    4- So I think your example is totally bogus.

  127. I was trying to find out what this alleged strawman was and you jumped in with some unrelated nonsense.

    So that is my point- evos like to throw around bald assertions and false accusations but are always very short on supporting evidence.

  128. Genome-wide analysis of a long-term evolution experiment with Drosophila

    A random search where the peaks and valleys change- good luck with that and your irrelevant population genetics equations…

  129. 1. Yes environments change (a little) and we can talk about that later if you want. But it’s not the issue you originally brought up

    2. That would just mean one of several possible beneficial mutations would get fixed.

    3. Yes it does.

    What do you think the chances of the beneficial allele fixing are? Just a range 0.1 – 1%?, 5%?

  130. 1- Environments change, sometimes quite a bit. What do you think ice ages did?

    2- Except beneficial is still a relative word

    3- No it doesn’t for reasons given above- one being even the most beneficial mutation can get lost in one generation.

    4- Experiments with stable environments do not support your equation:

    A random search where the peaks and valleys change- good luck with that and your irrelevant population genetics equations…

    And with a population of 10,000- your example- natural selection is a non-entity, so all you have left is sheer dumb luck

  131. Gish Gish Gish.

    I’m asking your for a estimate of the rate of fixation for an allele such as I described. If the fact that “even the most beneficial mutation can get lost in one generation” counts for much, natural selection is a non-entity in the population size in the scenario then we must be talking about a small number? Right?

    So what’s the number, roughly, do you think?

  132. Excuse me, but how is it possible for none of one parent’s genes to get passed on?

    You are right. I am getting confused about when recombination takes place.

    But the main point is what is the probability of new beneficial mutation being fixed in a population? It is possible for a beneficial mutation to be lost in one generation but the probability is low. The big thing you have left out is that parents on average have many offspring – in some species very, very many.

  133. wd400:

    (1) Williamson is crazy, there is no reason for a ‘Darwinist’ or anyone else to take him seriously.

    This is a very closed-minded view. Exactly the problem of Darwinists.

    Why don’t you just simply say: “I refuse to entertain such ideas.” (Of course, there’s no rational basis to this. You haven’t refuted Williamson’s contention.) I might not agree with Williamson’s views, but I would want to look at his evidence and his thought process. You’ve shown no such tendency. Is this how science is to be conducted?

    Of course, Shapiro is erecting a strawman there.

    Aren’t you guilty of the very thing you’re accusing Shapiro of? Haven’t you just made a strawman argument of Shapiro’s position. Haven’t you just thrown out all the substance and subtlety of his argument?

    As to “transition bias”, does such a thing actually exist? I cited a 2003 paper that suggests otherwise. And constraints such as “transition bias”, should it actually occur, happens at a chemical/quantum-mechanical level. Shapiro talks about “system engineering”. This represents a very different kind of “constraint”.

  134. Loser, loser, loser

    wd400:

    I’m asking your for a estimate of the rate of fixation for an allele such as I described.

    And I am asking for REAL LIFE examples- something which YOU will NEVER provide.

    Do you have anything dealing with the real world?

    I would say in your example the allele will never reach fixation and the fact is you cannot demonstrate otherwise.

    And that is the problem with your position-> it is untestable in the real world and relies solely on imagination.

  135. OK Mark- what % of offspriing will have the beneficial mutation and what % of those will have it on the dominant (as opposed to recessive) side?

    Heck Sir Ronald Fisher- one of the architects of the modern synthesis- he has shown that most mutatnts- even those with very beneficial effects, will be wiped out via random effects.

    Not only that there will be competeing mutants.

  136. Thanks very much for this, WD400, you’ve given me enough to go on here.

  137. Joseph,

    You really are a laugh. You started by saying sexual recombination meant “very beneficial” mutations can’t be fixed. But, in fact, even in the scenario I talked about with not very beneficial mutations and the chance of being lost in the first generation the probability that the newly arising allele is fixed in about 50%. Obviously it’s much higher for those “very beneficial” mutations you were talking about.

    If you want to see this for yourself download popG from Joe Felsenstein’s page and set up some populations.

    As for real world examples – there are thousands. But one I like is “Growth Advantage is Stationary Phase” (GASP). Take one cell, grow a few clones and split them into two dishes. Add the first colony to a flask of medium and it will grow unconstrained until it reaches the end of the resources and reaches “stationary phase” where the number of cells in the flask reaches equilibrium. That’s a dynamic equilibrium, cells are dieing and others are reproducing and eating the remains of other cells.

    Now. Take some of those cells that have already been in stationary phase and an equal number of cells from the other cloned colony you had to start with and grow them up into another stationary phase. If mutations are unlikely to prosper, then there is no reason to think either colony will do better than the other. But every time the cells that have already been through a stationary phase out compete their counterparts and when you sequence the cells you find fixed mutations that arise in their earlier stationary phase that made them fit their environement (remember, they were clones, so it can’t be existing differences).

    Not that I suppose anything can change your mind about how right you are though.

  138. wd400:

    You started by saying sexual recombination meant “very beneficial” mutations can’t be fixed.

    No, I did not say that.

    But, in fact, even in the scenario I talked about with not very beneficial mutations and the chance of being lost in the first generation the probability that the newly arising allele is fixed in about 50%.

    Too bad you don’t have any real world evidence that supports your claim. You don’t even have experimental evidence.

    IOW all you have is your bald assertion.

    OTOH I have provided a peer-reviewed paper that supports my claim.

    Take one cell, grow a few clones and split them into two dishes.

    LOSER- what part of sexual reproduction don’t you understand?

    But anyways thanks for proving that you don’t have any clue nor do you have any positive evidence for your claims.

  139. Did you read this paper. New mutations increased the fitness of their holders. In a sexually reproducing species.

  140. Yes I read the paper- no new alleles became fixed.

    I never said mutations cannot increase fitness- which is a total BS term wrt biology anyway- but the fact that even mutations that increased fitness did not become fixed, supports my claim.

  141. But some did become fixed and others moved from 1/population.size to like 0.8

    So… sexual recombination doesn’t prevent new mutations from being selected for.

    Try again.

  142. You are just confused.

    First I said sexual reproduction- I never said anything about the recombination that can take place during meiosis.

    Next I never said anything about new mutations not being selected for.

    Please reference the new alleles that became fixed.

    try again, indeed…

  143. wd400:

    Imagine a population of 10 000 fixed for an allele we’ll call “-”. A new mutation pops up making the allele “+”, and the finesses are

    “-/-” : 0.98
    “+/-” : 0.99
    “+/+” : 1.0

    So, to start we would have 9999 individuals with “-/-” and 1 with “+/-”.

    That would mean the +/- would be mating with a -/-.

    How many of their offspring would have the “+” allele? How can you tell?

    How many offspring would they have to have to ensure ONE “+” allele gets passed on?

    What happens when the -/- the one +/- mated with has deletrious alleles?

    The point being, as I have already eluded to, is your equations do not deal with reality.

  144. Next I never said anything about new mutations not being selected for.

    You said they’d be lost. But in fact they arise and a lot of them become very commmon (like 0.8)

    Please reference the new alleles that became fixed.

    See the dots with allele frequency = 1 in their graphs? For both methods of calling genotypes? Those are fixed allles.

  145. Next I never said anything about new mutations not being selected for.

    wd400

    You said they’d be lost.

    I never said anything about new mutations not being selected for.

    Also, from the paper:

    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.

    YOU LOSE.

    And becoming common does not mean becoming fixed. And that was under controlled lab conditions which means in the wild you lose too.

  146. Our work provides a new perspective on the genetic basis of adapta- tion. 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 is notable because in wild populations we expect the strength of natural selection to be less intense and the environment unlikely to remain constant for,600 generations. Consequently, the probability of fixation in wild populations should be even lower than its likelihood in these experiments. This suggests that selection does not readily expunge genetic variation in sexual populations, a finding which in turn should motivate efforts to discover why this is seemingly the case.

    OOOPS….

  147. How many of their offspring would have the “+” allele? How can you tell?

    High school math? The expectation is half of the offspring, with variance n/2*(0.5) where n is the number of offspring.

    How many offspring would they have to have to ensure ONE “+” allele gets passed on?

    4 would give you a 94% chance

    What happens when the -/- the one +/- mated with has deletrious alleles?

    Well, that’s the thing about sex isn’t it. The alleles get broken up every generation. But that’s all gish anyway, it wasn’t part of your orignal claim, only added on when you started to realise your confidence was misplaced.

    The point being, as I have already eluded to, is your equations do not deal with reality.

    They do. It’s ok to be wrong. Just stop, and think about it. Do you really think every evolutionary biologist in the world is unaware that newly arising mutations can be lost in the first generation. Or maybe that they’re aware of it, thought about it, tested it and, in the case of the nearly neutral theory, built new theories about it.

  148. Well, I’m happy to admit I read that paper wrong. Seems the only alleles that were fixed were ones that already existed in the population.

    But that doesn’t really help with your case. If (a) selection can get new mutations into populations and up to a decent level and (b) selection can drive existing alleles to fixation then it follows newly arising alleles can go to fixation!

    Moreover, non-adaptive alleles can (and do) go to fixation. In fact, for a neurtral allele the the rate of fixation is equal to the mutation rate. Selection just makes that go faster. Quite a lot of population genetics is about comparing the rate of substitution rate to mutation rate to see if alleles are fixed faster than mutation would allow.

  149. How many of their offspring would have the “+” allele? How can you tell?

    High school math?

    Nope- reality.

    The expectation is half of the offspring, with variance n/2*(0.5) where n is the number of offspring

    Doubtful. Do you have any real-world data to support your claim?

    How many offspring would they have to have to ensure ONE “+” allele gets passed on?

    4 would give you a 94% chance

    And the evidence to support your claim is?

    What happens when the -/- the one +/- mated with has deletrious alleles?

    Well, that’s the thing about sex isn’t it. The alleles get broken up every generation.

    Non-sequitur.

    But that’s all gish anyway, it wasn’t part of your orignal claim,

    You don’t have any idea what my original claim was as you have trwisted it with most of your posts.

    only added on when you started to realise your confidence was misplaced.

    My confiemce is still high and you have yet to provide any evidence to support your nonsense.

    The point being, as I have already eluded to, is your equations do not deal with reality.

    They do.

    No, they don’t.

    Do you really think every evolutionary biologist in the world is unaware that newly arising mutations can be lost in the first generation.

    Has any biologist applied the equations to a population in the wild?

    We have to a population of fruit flies and no new alleles became fixed- YOU LOSE.

  150. If (a) selection can get new mutations into populations and up to a decent level and (b) selection can drive existing alleles to fixation then it follows newly arising alleles can go to fixation!

    “Ifs” don’t help your case. Imagination doesn’t help your case. And unfortunately those are all you have.

    Moreover, non-adaptive alleles can (and do) go to fixation.

    Evidence please.

    Quite a lot of population genetics is about comparing the rate of substitution rate to mutation rate to see if alleles are fixed faster than mutation would allow.

    Quite a lot of population genetics takes place on paper and does not translate to the real world.

    As for “selection”, well nature doesn’t select- natural selection is an oxymoron.

  151. So, what you are saying is you are so convinced you are right you are willing to deny the Binomial Theorem (the source of those numbers)?

    I’m going to back away slowly now.

  152. You are going to back away because you cannot support the nonsense you post.

  153. Joseph, s/he just did. It’s just math (though the math is quite complicated!)

    Check out Kimura’s classic paper here.

  154. Elizabeth-

    The math just shows the distribution of gametes. It does NOT show the distribution of offspring.

    Also as far as getting a new allele fixed wd400 choked on that. She/ he also choked on the fact that even someone carrying a beneficial mutation will most likely pass on deletrious mutations as well.

  155. OK Joseph, one last go.

    The math just shows the distribution of gametes. It does NOT show the distribution of offspring.

    Nope. The maths is explicitly about diploid populations with sex. Amusingly enough, you can actually get the expected offspring distribution form the gamete distribution.

    But in the really simple case above. I’m sure you’ll agree the probability that any offspring receives any given allele is 0.5 right? Doesn’t matter it’s “+” “-” or “blue eyes” or whatever – parents have two each offspring gets one. That means half of a mutants offspring will have the the newly arising allele.

    You wanted to know how many offspring you’d need to be sure to get the “+” into the next generation, and that’s pretty easy maths too. The probability of offspring1 and offspring2 having the “+” is independent (different eggs or sperm) so you can mulitly them. So, the chance of getting 4 “-”s in a row is 0.5^4 ~ 0.06 and the probability of getting at least one “+” is 1-0.06 = 0.94.

    I don’t know why you think background deleterious alleles are a problem here. Individuals with a new beneficial mutation have no more or less chance of having a bad one somewhere else. Moreover, sex means genes get broken up by recombination, so selection acts on individual genes.

    Finally, I’m happy to admit I read a graph in that paper incorectly. But that paper as a whole doesn’t support your claim since (a) newly arising mutants can become quite common (b) quite common alleles can go to fixation. From that it follows mutations can go to fixation. And as I said, non-adaptive alleles go to fixation (read the Kimura paper). If they didn’t, how would fixed differences between populations or species come about?

  156. wd400,

    What is umm “expected” is NOT what always happens.

    Also “selection” does not “act” on anything- natural slection is an oxymoron and a result of three processes- an after-the-fact assessment.

    What is your evidence that newly arising mutatnts can become fixed? I don’t care about “quite common” that is BS backpeddling.

    And i did NOT say new mutations will never become fixed. I said they are unlikely to become fixed. And the data supports my claim. OTOH you don’t have any data to support your claims.

    As for delitrious mutations, well they tend to wipe out and “benefit” of the beneficial one.

    How did fixed differences come about? By design, as they were designed in.

Leave a Reply