@JamesPlaskett Protesting too much: no spontaneous beneficial mutations?

James Plaskett has been directing us to the anti-Darwinian writings of Richard Milton in support of the claim that there are no spontaneous beneficial mutations.

The go-to experiment for beneficial mutations is undoubtedly the very long and painstaking work led by Richard Lenski, which showed the spontaneous appearance of bacterial lines able to metabolise citrate. These are generations raised in over twenty years of research in which samples are frozen, where the appearance of a mutation can be demonstrated to arise and arise repeatedly, and these mutations are not merely the ready re-expression of a formerly dormant capacity.
http://en.wikipedia.org/wiki/E._coli_long-term_evolution_experiment#Evolution_of_aerobic_citrate_usage_in_one_population
But I don’t think Milton was aware of that instance when he wrote.  Then, the classic case was antibiotic resistance in bacteria:

“For instance, from a single bacterium one can grow a population in the presence of an antibiotic, and demonstrate that organisms surviving this culture have mutations in genes that confer antibiotic resistance. In this case (in contrast to the situation with the peppered moth populations described above) origin of the population from a single bacterium allows comparisons of the mutated genes with the corresponding genes from the original bacterium, verifying that the variant sequences were not present before the culture with antibiotics and therefore arose as de novo beneficial mutations.”

Edward Max, http://www.talkorigins.org/faqs/fitness/ 1.2.1

Let’s turn to Milton’s objections  (which have fallen off the web, but I presume Milton still stands by them):

“This claim can never be strictly true. In order to do what Dr Max describes here, the experimenter would necessarily have to both culture the new population from his single experimental bacterium AND fully sequence the DNA in that same single bacterium for later comparison. But, of course, analysing the DNA of the experimental bacterium must necessarily destroy it, making it impossible to culture from.
“Instead the experimenters do the next best thing: they select a number of individuals from the same culture, which they assume to be genetically identical and they analyse the genes of one (or more) and use the others to culture the new colony. If the bacterium they select to analyse appears not to have any genes for antibiotic resistance then they assume that the same must be true for its close relative they are using to breed.”

http://web.archive.org/web/20041012235607/http://www.alternativescience.com/talk.origins-antibiotic.htm

I think that ‘genetically identical’ assumption is a good one, and can also be shown to be true. Because these are bacteria arising from asexual reproduction of a single cell (a routine microbiological technique), they are all necessarily genetically identical ‘twins’ and will remain so until the appearance of any mutations. You can sample from the population to show that whatever it takes to be resistant to an antibiotic is not there at one point and is there at a later point.

You can even see this in real time. A bacterial population with a single founder will spread across a plate up a gradient of increasing antibiotic concentration until they are brought to a halt by the antibiotic. After a pause, suddenly and spontaneously, they break through to the neighbouring area of the plate which was previously uninhabitable.  (I seem to remember seeing that on Bang Goes The Theory earlier this year.)

“Despite Dr Max’s denials, the case of antibiotic resistance in microorganisms is exactly the same in principle as that of so called ‘industrial melanism’ in the peppered moth. It is simply a case of one variety of the species flourishing while another variety dies off, because of changed environmental conditions.”

I think that shows that Milton hasn’t understood the power of the single-founder experiments. There is only one variety to start with.

Elsewhere:

“…It is perfectly feasible that many bacteria possess genes that can provide resistance — whether or not those genes are currently expressed, and whether or not they have even been identified by geneticists as genes for providing antibiotic protection. Such unexpressed genes are known to be sometimes ‘switched on’ by environmental pressures of just the life-threatening kind that are applied to bacteria in the lab. So, even if antibiotic resistance were genuinely arising during the experiment, it is not necessarily arising de novo, as Dr Max claims, but may merely be a genetic throwback.”

It may be the work hasn’t been done to exclude this possibility in every case, but certainly there are many examples of single changes in DNA sequences that produce antibiotic resistance.  These cases are not due to the turning on of an unexpressed pre-existing capacity, these are spontaneous beneficial mutations in a gene expressed throughout (http://aac.asm.org/content/44/7/1771.full).

The Lenski team has also nailed what is going on in their experiments, and it too is certainly not the recovery of a previously unexpressed capacity.

Milton also offers:

“Perhaps Dr Max and other convinced Darwinists might say that choosing one bacterium for genetic analysis and a very close relative for culturing is as close as one can get to experimental certainty, and is almost scientific proof. But the whole point of science is that ‘almost’ isn’t good enough.”

Although I think the lab work is immune to the criticisms Milton offers, I think this statement is also worth challenging: it is a misconception about the nature of science.   As close as you can get to certainty is as close as you can get, and if you demand a higher standard, you are demanding, not just proof beyond reasonable doubt, but proof beyond unreasonable doubt. And that’s Milton’s problem, not a problem with the neo-Darwinian synthesis.

Reflection: It’s actually enough for only one element of the neo-Darwinian synthesis to fail: for mutations to be too uncommon or never beneficial, or for natural selection never to be observed in or out of the lab., nor mating barriers; or for the molecular tree to contradict the morphological tree, or for some other prediction to be disproved… And yet it seems Milton wishes to dispute every little bit of it. He protests too much.

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6 responses to “@JamesPlaskett Protesting too much: no spontaneous beneficial mutations?

  1. MANY points raised!

    To start with antibiotic resistance and the claims of yourself + Señor Ford that it has been observed.

    The scientific problem is to account, empirically, for the observed fact that some bacteria such as Staphylococcus have become more resistant to antibiotics over time. There are two competing explanations:

    1) The less resistant individual bacteria are being killed off, leaving a higher concentration of the more resistant strain.

    2) The normal strain, through mutation, is becoming more resistant to antibiotics.

    The experiments conducted to discriminate between these two competing explanations are claimed (by Darwinists) to have settled the matter in favour of theory 2. Some Darwinists also claim the experiments provide empirical evidence of evolution in action. Both claims are wrong.

    Researchers sequence the DNA of a bacterium, observing that it does not contain the gene that resists an antibiotic. Then they grow a culture from another bacterium from the same batch – assuming that the resulting culture must be free of the antibiotics-resistant gene. They then introduce antibiotics to the experimental culture. If some bacteria then resist antibiotics, they conclude A) that antibiotic resistance has arisen through mutation and B) this is evolution in action.

    The first conclusion is false because researchers are necessarily destroying the bacteria whose DNA they sample and then merely assuming that the bacteria they culture from the same batch are also free of antibiotic resistant genes. I sympathise with the point of view that it is a “reasonable assumption” but science isn’t about reasonable assumptions – it’s about empirical evidence providing conclusive evidence.

    The second conclusion is false because evolution is about one species changing into another species. Even if it were true that bacteria were undergoing genetic mutation to become antibiotic-resistant, this would not assist Darwinists. The bacteria would not be turning into a new species (and indeed it is interesting to note that microbiologists have not in fact erected new species to take account of such trivial differences). And second, the Darwinian mechanism postulates the natural selection of random genetic mutations. This – if proved – would be a case of a mutation arising not at random but in a directed way – something that is antithetical to Darwinist beliefs.

  2. @JamesPlaskett Thanks for the reply. In Tweet-size bites: 1/4 No-one claims scientific ideas require absolute proof, except you and Milton

    2/4 Milton: “the experimenters … select a number of individuals from the same culture” – wrong – just one founding cell

    3/4 Bacteria in those experiments really are identical twins of each other, founded by a single cell- so only ever one “strain” to start with

    4/4 No-one is claiming antibiotic-resistant bacteria are new species, but that species arise by the same process of natural selection

  3. P.S. We do know the random mutation rate for the genes in question, and it’s sufficient to account for the experimental evidence http://aac.asm.org/content/44/7/1771.full

  4. Well, this isn´t a comprehensive response to all of the challenges you threw at me.
    But it´ll do, I guess, for openers –

    To start with antibiotic resistance and the claims of yourself + Señor Ford that it has been observed.

    The scientific problem is to account, empirically, for the observed fact that some bacteria such as Staphylococcus have become more resistant to antibiotics over time. There are two competing explanations.
    1) The less resistant individual bacteria are being killed off, leaving a higher concentration of the more resistant strain.
    2) The normal strain, through mutation, is becoming more resistant to antibiotics.

    The experiments conducted to discriminate between these two competing explanations are claimed (by Darwinists) to have settled the matter in favour of theory 2. Some Darwinists also claim the experiments provide empirical evidence of evolution in action. Both claims are wrong.

    Researchers sequence the DNA of a bacterium, observing that it does not contain the gene that resists an antibiotic. Then they grow a culture from another bacterium from the same batch – assuming that the resulting culture must be free of the antibiotics-resistant gene. They then introduce antibiotics to the experimental culture. If some bacteria then resist antibiotics, they conclude A) that antibiotic resistance has arisen through mutation and B) this is evolution in action.

    The first conclusion is false because researchers are necessarily destroying the bacteria whose DNA they sample and then merely assuming that the bacteria they culture from the same batch are also free of antibiotic resistant genes. I sympathise with the point of view that it is a “reasonable assumption” but science isn’t about reasonable assumptions – it’s about empirical evidence providing conclusive evidence.

    The second conclusion is false because evolution is about one species changing into another species. Even if it were true that bacteria were undergoing genetic mutation to become antibiotic-resistant, this would not assist Darwinists. The bacteria would not be turning into a new species (and indeed it is interesting to note that microbiologists have not in fact erected new species to take account of such trivial differences). And second, the Darwinian mechanism postulates the natural selection of random genetic mutations. This – if proved – would be a case of a mutation arising not at random but in a directed way – something that is antithetical to Darwinist beliefs.

    1) Cytochrome C.
    You say that your first impression upon seeing the patterns of cytochrome c
    was that it as so clear cut as to be an obvious support of neo-Darwinian thinking.

    Well, the first retort is that these DNA similarities may be doing no more than to reflect the similarities which greet the eye.
    A general pattern for four-limbednes one would expect to find in all creatures with four limbs.
    Irrespective of how they came to be.

    You´ve challenged me to cite references to divergent DNA patterns within similar creatures, e.g. frogs.
    Still working on that and on trying to contact Denton personally re teh volte-face of his you cited…

    2) Natural Selection

    I have never said that natural selection was “unlikely”, and am indeed uncertain even what that phrasing could be taken to mean.
    You must have misunderstood something.

    Complex structures Evolution of complex structures is too unlikely (e.g. the eye as cited by Grasse) Taking what is generally regarded as a useful test case, the evolution of the eye, and making some conservative assumptions (1% change in proportion arises by mutation, mutations happen at observed rates, 1829 1% steps are required, modest selection pressure applies),

    3) “Mutations happen at observed rates…”
    Do they now?
    Only favourable mutations have any relevance to that argument, as you very well know.
    And what rates are those?
    Consider the speculations of Julian Huxley and French biologist Jaques Monod. Huxley estimated that the rate of inheritable mutation was around one in every million births. Monod estimated it at one in ten thousand births. The reason for this diversity of opinion between the Professor of Zoology at King´s College, London and the director of Paris´s Pasteur Institute is simple; it is because the beneficial spontaneous mutation remains no more than a hypothetical necessity to the neo-Darwinian theory.

    Darwinists try to get around the problem of rate of favourable mutation by a number of dodges: –
    a) They include amongst the figures for observed mutation examples of conditions which could not possibly favour an organism such as Huntingdon´s corea, Downs´ syndrome, cystic fibrosis, dwarfism, etc, although nobody wants these.
    b) They confuse sub-specific variation with mutation, forgetting that this can never need to novelty in form above the species level. This is what you are trying to do by citing a different coloured moth as an example of favourable mutation.
    c) The maths argument of Dawkins, dubbed by Nobel laureate Crick The Statistical Fallacy. Dawkins claims that breaking down the development of a complex structure via cumulative mutation into lots of little steps reduces the improbability of it coming about in one go.
    Crick pointed out that this is simply mathematically false.

    “…the maths suggest that there has been time for a complex eye to have evolved from scratch – time indeed, for it to evolve, not just once, but 1500 times in a row (Nilssen and Pelger 1994).”

    You conclude here with
    “…If you want to disbelieve, I can’t stop you, but if you want to disagree, you may have to roll your sleeves up and do some maths. (I confess the maths may be beyond me.) ”

    The maths is terrifying. Not in its difficulty but in its implications.

    Not that I want to disbelieve.
    I find myself having to agree with Prof. Pierre Grassé, who for 30 years held the chair in Evolution at the Sorbonne.
    Where is the gambler, however obsessed with his passion, who would be crazy enough to bet on the roulette of random evolution?
    The creation, by grains of dust carried by the wind, of Dürer’s Melancholia has a probability less infinitesimal than the construction of an eye through the mishaps which might befall the DNA molecule – mishaps which have no connection whatsoever with the future functions of the eye.

    The maths is so ludicrous that to believe in what you seem to regard as an essential part of the philosophy of any modern thinking person requires an almost religious confidence in truly astronomical levels of improbability.
    (And i am afraid that your adding in your last P.S that we “do know the random mutation rate for the genes in question…” is, I am sorry, absurd.)
    4) No Speciation Event Yet Observed
    If you want to suggest that polyploids are instances of true speciation then we waste our time in debate.
    The diversity of the plant and animal kingdoms came about by no more than freak doubling of DNA-sometimes all of it?
    Be reasonable, please.

    And when did Dobzhansky abandon the Strong Species Definition, please?

    To argue that Boxhorn´s stuff “could” be leading to speciation is all very well.
    But the FAQ is headed
    Observed Instances Of Speciation, is it not?

    5) Useful Mutations Never Happen
    Two observations re the initial stuff you posted re claism of observed favourable mutation in bacteria:

    First “The database is currently undergoing restructuring and data valuation” so the claimed evidence is not in fact available.

    Second, the only experiment that could, without doubt, prove mutation in response to antibiotics is a physical and logical impossibility. The “evidence” claimed is in fact an inference not empirically determined as claimed.

    You cite the darkened type of Peppered Moth as an example of a mutation sometimes proving useful.
    But you have no idea how it darkened in the first place.
    How do you know any mutation ever caused that?
    An assumption.
    Rational enough certainly. But still an assumption.

    Your whole world view rests upon useful copying errors in genes.
    Doesn´t it?
    Throughout this 15 minute elementary exposition the presenter does not once confront the most important truth: none of the instances of spontaneous mutations he cites could possibly benefit anyone.

    6) Complex Life cycles

    I said that my two initial problems with evolution via natural selection of cumulative mutation were the improbability and the irrelevance.
    Both of those apply fully to this objection.
    You say that it´s something new for you.
    Startling.
    If you don´t think the metamorphoses of a butterfly pose any major kind of challenge to your world view then this truly is a dialogue of the deaf and we really are both wasting our time.

    Oh: look how the Halipegus worm reproduces!
    – a parasite in Nebraska, a flatworm called a trematode (Halipegus eccentricus), that scientists discovered living in the ears of bullfrogs. But the trematodes in their ears are all adults.
    Matt Bolek from the University of Nebraska described how he and colleagues figured out the rest of the parasite’s life cycle.
    The parasites release their eggs from the frog ears, which then get scarfed up by snails, where they hatch and start to develop. Then they leave the snails and swim in search of little aquatic invertebrates called ostracods. The ostracods get eaten by the larvae of damselflies, which then mature and fly into the air, only to be devoured by frogs. The parasites escape the damselflies and move through the bodies of the frogs to their ears.
    One trematode, four hosts.

    And Halipegus´ life cycle sits comfortably with the gradual assimilation, over millions of years, of useful accidental changes, eh?

    I don´t think so.

    7) Convergent evolution: Doppelgangers

    You say that you have not heard of the challenge of the doppelgangers of Australia before.
    Startling.
    For many of us the appearance in isolated environs of the same thing – only difference is reproductive system -is amongst the strongest possible evidence that natural selection of spontaneous mutations is not what wrought the forms and also amongst the strongest possible evidence that some other unknown process or processes must have been involved.
    YOU regard it as amongst the clearest corroborations of your beliefs.
    George Gaylord Simpson said that natural selection of mutations and adaptation to environment was the explanation of the doppelgangers.

    Arthur Koestler responded “You might just as well say that there is only one way of making a wolf which is to make it look like a wolf.”

    Right.
    You seem to have colossal optimism that every now and again a change for the better will be dished up via spontaneous mutation.
    This confidence we do not share.
    It´s wishful thinking, not observation.

    Would you care to comment on the absence of transitional fossils in the Antipodes for these mirror images, Dr?
    Or, to my way of thinking far more cogently still, the absence of aberrant fossils en route to the doppelgangers.
    Each step of the way the next novelty may be anthing. Anything at all. Where´s the fossil evidence for all of these losing tickets, then?
    Satisfied with nothing more than – Hey Presto! – the finished doppelgangers, are you?

    re Convergence and how I think it´s amongst the most powerful evidence against neo-Darwinism and people like yourself think it amongst the most corroborative – here´s Prof. Jerry Coyne –
    Perhaps the most astonishing example of convergence is the similarity between some species of marsupial mammals in Australia and unrelated placental mammals that live elsewhere. The marsupial flying phalanger looks and acts just like the flying squirrel of the New World. Marsupial moles, with their reduced eyes and big burrowing claws, are dead ringers for our placental moles. Until its extinction in 1936, the remarkable thylacine, or Tasmanian wolf, looked and hunted like a placental wolf.
    Convergence tells us something deep about evolution. There must be preexisting “niches,” or ways of life, that call up similar evolutionary changes in unrelated species that adapt to them. That is, starting with different ancestors and fuelled by different mutations, natural selection can nonetheless mold bodies in very similar ways–so long as those changes improve survival and reproduction. There were niches in the sea for fish-eating mammals and reptiles, so porpoises and ichthyosaurs became streamlined. Animals in the Arctic improve their survival if they are white in the winter. And there must obviously be a niche for a small omnivorous mammal that glides from tree to tree. Convergence is one of the most impressive features of evolution, and it is common: there are hundreds of cases.
    Incredible stuff.
    The guy just bats away the phenomenon and presses the doubling of improbability into service in support of his worldview!
    8) Natural selection too slow

    That was not the point of Crick and Milton.
    The point was that the breaking down of the creation of something very complex into lots of little steps reduces the unlikelihood of it all happening at once.
    This argument helped him to win an award for top science on TV when he put it forward in defence of neo-Darwinism on Horizon in 1975.
    No objection from Crick re speed per se.
    The 2010 defence of how gradual assimilation via cumulative favourable mutation becomes less improbable if simultaneous alterations are occuring in different parts of the process Milton and I challenged because of its unrealism and non-reduction of improbability.
    I repeat my 1st problem in a book that you take as Gospel: Climbing Mount Improbable.

    No human investigation can be called true science without passing through mathematical tests.”
    Leonardo da Vinci

    One of the biggest headaches I have with what you believe in is the absence of evidence for Natural Rejection.
    We are told, e.g. by Jostein Gaarder in Sophie´s World, that the living world around us is comprised of winners in a lottery of life.
    Where then is the evidence for all of the losers?
    Once again we find ourselves drawn towards a consideration of the rate of mutation.
    Even the most ardent defender of neo-Darwinian theory concedes that useless or positively harmful mutations enormously outnumber good ones. (I think there have been no good ones yet seen!)
    So one corollary of what you say is so crystal clear ought to be a huge pile of discard material in the fossil records.
    It is not enough to win; others must also lose. This is the very essence of the Darwinian concept: the triumph of favoured races in the struggle for survival.
    Again the maths is clear and awesome. Each step of the way the useless mutations ought to be being generated in vast numbers and then, via your logic, being naturally rejected.
    But the records show us nothing like that.
    This Blind (and mindless) Watchmaker would appear to have hit upon a functioning watch every single time (every single fossil.)
    It might be disparaged as a Mickey Mouse contraption by contrast with today´s gold plated Rolex but it is still a watch, i.e. we may envisage it working.
    This is the last pattern one would expect of a theory which postulates and relies upon random generation of novelty and some of the clearest evidence you could ask for to indicate that if evolution occured then the mechanism driving it was not the neo-Darwinian one.

    Nature of science ‘Probably’ is not good enough ‘Probably’ is as good as you get; certainty is for mathematicians (and theologians).I wouldn’t offer anything in science as absolutely ‘certain’ or ‘indisputable’. (We were pretty sure about Newtonian mechanics, but that turned out to be at best a useful approximation and seriously flawed if you want your GPS to work.) I would offer natural selection as the best current scientific explanation we have for most* examples of adaptation and speciation.
    * Genetic drift is the best explanation of the cytochrome c ‘bush’, sexual selection is the best explanation of the peacock’s tail, and so on.

    ….and the life cycle of the butterfly and halipegus (amongst a zillion other examples of behaviour and features which any honest mind would find well nigh impossible to fit with your idea of truth, i.e conserved adaptive lucky accidents.)(?)

    Lastly, you have posted here about why people believe in strange things, prompted by my anti-Darwinism.
    Look at the list of problems here mentioned -and you´ll find many, many more in a compendium critique like Milton´s Shattering The Myths of Darwinism – and please permit yourself to entertain the idea that it is the defenders of modern evolutionary theory who are exhibiting irrationality!?

    You say Milton is simply making too many objections.
    That´s only because he attempted in his book a global critique of neo-Darwinism.
    In 1981 Gordon Rattray Taylor – man who, like Milton, did believe in evolution – wrote of as many anomalies in his The Great Evolution Mystery.
    And the writings of Norman Macbeth and Arthur Koestler.
    There are far, far more objections to neo-Darwinian theory than you´ll find at Milton´s or any other blog.

    James

    • Thanks for taking the time to comment again, I do appreciate
      it. 

      I shall try and be as brief as I can in reply, for fear of having
      to write a book-length rebuttal; I apologise in advance if that
      comes across as brusque in places.

      Spontaneous beneficial mutations/antibiotic resistance

      HJP: Researchers sequence the DNA of a bacterium,
      observing that it does not contain the gene that resists an
      antibiotic. Then they grow a culture from another bacterium from
      the same batch – (…)

      DR: This is wrong. I notice you have changed way you describe
      these experiments from Milton’s original wrong description, but
      it’s still wrong.

      Let me have another go, and you tell me which step is a problem
      for you:

      1. These studies are done using single-cell-founded colonies,
        from cultures that are susceptible to antibiotics,
      2. so the bacteria are all identical twins with identical genes
        to start with,
      3. and so are all identically susceptible to antibiotics, 
      4. and when you go back later and see what they are doing, you
        find some can resist antibiotics,
      5. so they are clearly no longer identical,
      6. and if you can tell that they are not contaminated (because of
        other genetic markers and indeed, no appearance of other species
        on the plates),
      7. then the new resistant forms must have arisen by
        mutation. 

      These are therefore, repeated, spontaneous, beneficial mutations,
      and I really cannot understand why you won’t accept them as
      such. 

      Please note that the argument thus far doesn’t depend on DNA
      sequencing at all!  But if you do look at the molecules, you
      can see how the resistance arises on different occasions and in
      different species, and that’s where a lot of the research is now
      going on, and to which I pointed you.

      If we turn away from antibiotic resistance, Lenski’s experiment
      with evolving bacteria  is hugely impressive — it has shown
      the rise of many, many different mutant forms within colonies
      which were founded thousands of generations before by single
      cells. The appearance of bacteria able to metabolise citrate was a
      celebrated instance, but then Lenski and his team went back to the
      parent generations that
      had been frozen, and showed that this new ability to metabolise
      citrate could and would arise again.  Again, repeated,
      spontaneous, beneficial mutations.  [Which is the point —
      no-one argues that this is speciation, a red herring in this
      context.]

      HJP: I sympathise with the point of view that it is a
      “reasonable assumption” but science isn’t about reasonable
      assumptions – it’s about empirical evidence providing conclusive
      evidence.

      DR: I was being ironic.  It’s not a ‘reasonable assumption’,
      it’s a provable consequence of how they actually do the
      experiments.  If you start with a single cell, they will all
      have the same genetic makeup to start with [(2) above]. 

      Cytochrome c: molecular evidence for common ancestry

      HJP: 1) Cytochrome C.
      You say that your first impression upon seeing the patterns of
      cytochrome c was that it as so clear cut as to be an obvious
      support of neo-Darwinian thinking.

      Well, the first retort is that these DNA similarities
      may be doing no more than to reflect the similarities which greet
      the eye.
      A general pattern for four-limbednes one would expect to find in
      all creatures with four limbs.

      DR: Please note that cytochrome c is not made out of DNA, it’s a
      protein made out of a chain of various amino-acids, found in the
      mitochondria of cells.  We can construct a detailed and
      consistent ‘tree’ of relationships based on the amino acid
      sequence of cytochrome c (and other molecules, including RNA and
      DNA).  This is required by neo-Darwinian theory and has been
      found.  That’s as much as the argument needs to do. 

      Your argument about ‘reflecting similarity’ is too vague, and
      insufficient to chase off the evolutionary conclusion.  Why
      should dolphins have a cytochrome c that is more similar to a
      bat’s than a shark’s?  Why should obscure details in of tiny
      parts of a protein in a tiny part of a cell, which does exactly
      the same job in every four-limbed creature (indeed, the same job
      in everything more complicated than a bacterium), fit a family
      tree?  Remember, the differences in fact make no difference
      to function, since you can take the cytochrome c out of a mammal
      and put it in a yeast and the yeast still functions.  This
      molecule clearly has nothing to do with how many legs you have, or
      even whether you have one cell or many.  So why are these
      molecules different at all?  There is no reason why the
      external, visible similarities of various groups of vertebrates
      should be matched with shared similarities in the non-functional
      elements of cytochrome c (and every other molecule we look at),
      and no reason why these pointless differences should be consistent
      with each other and everything else we look at within a group,
      unless members of that group all descended from a common
      ancestor.  It’s just the simplest explanation of the
      findings.  [It doesn’t matter to me too much whether Denton
      still believes whatever half-baked ideas he originally proposed to
      explain away the cytochrome c story; it was clearly bogus at the
      time but the molecular evidence has been so massively developed
      since then that any competing explanation will have to do a lot
      more work – too much work, I believe.]

      And do please recall that we sometimes see large-scale visible
      similarities in animals which are contradicted by both molecular
      evidence and skeletal evidence, yet then the skeletal evidence
      matches exactly the molecular evidence.  For example, seals
      are most similar to manatees in how they ‘greet the eye’, but
      bones and molecules both place seals with bears and weasels, and
      manatees with elephants and hyraxes.  No other theory even
      suggests that this is likely, let alone inevitable, and yet we
      find it.  The evidence is all shouting at us as loud as it
      can, “common ancestry”. 

      Rates of beneficial mutations

      HJP: 3) “Mutations happen at observed rates…”
      Do they now?
      Only favourable mutations have any relevance to that argument, as
      you very well know.
      And what rates are those?

      DR: I previously offered http://aac.asm.org/content/44/7/1771.full,
      a review by Martinez and Baquero, which gives links to many papers
      which give estimates of what actually happens.  The mutation
      rates of favourable mutations leading to resistance to antibiotics
      in many different bacteria are in some sense known, but in
      studying them, we also know that the rates can rise and fall (“the
      specific mutability for a single base can vary by more than
      10,000-fold”).  You had some fun in your comments with
      estimates produced before the modern era of molecular biology, but
      I think you’re going to have to give up that particular pleasure.

      I promise you, Jim, the statistics are not on your side. 
      Let me offer you this, about Staphylococcus (the MRSA
      bug):

      “With a genome size of 2.8 × 106 and a
      mutation rateof 1 mutation per 1010 base pairs, it
      would take a single bacterium 30 hours to grow into a population
      in which every single base pair in the genome will have mutated
      not once, but 30 times! Thus, any individual mutation that could
      theoretically occur in the bacteria will have occurred somewhere
      in that population—in just over a day.”
      http://www.nature.com/scitable/topicpage/antibiotic-resistance-mutation-rates-and-mrsa-28360

      Statistics and probability

      HJP: (…) c) The maths argument of Dawkins, dubbed by
      Nobel laureate Crick The Statistical Fallacy. Dawkins claims that
      breaking down the development of a complex structure via
      cumulative mutation into lots of little steps reduces the
      improbability of it coming about in one go.
      Crick pointed out that this is simply mathematically false.

      DR: Progress by steps does reduce the probability if you are
      allowed to ‘bank’ progress so far, and as long as each
      intermediate position is has an advantage over previous models,
      that’s what will happen in the gene pool.  It’s like a
      rachet.  It makes apparently improbable events, not just less
      improbable, but actually likely.

      I have recently found the description of the ‘Statistical
      Fallacy’ in Chapter 7 of Crick’s 1981 book ‘Life Itself’, and I
      can tell you that his discussion in that book is not only
      different to what you describe, it also has nothing to do with the
      evolution of species by natural selection.  [Crick was a
      lifelong Darwinist; surely that tells you that his argument
      doesn’t have the power you are crediting it with?]

      HJP: Not that I want to disbelieve.
      I find myself having to agree with Prof. Pierre Grassé, who for 30
      years held the chair in Evolution at the Sorbonne.
      Where is the gambler, however obsessed with his passion, who would
      be crazy enough to bet on the roulette of random evolution?
      The creation, by grains of dust carried by the wind, of Dürer’s
      Melancholia has a probability less infinitesimal than the
      construction of an eye through the mishaps which might befall the
      DNA molecule – mishaps which have no connection whatsoever with
      the future functions of the eye.

      DR: You have previously quoted the maverick Grassé to me, and his
      wonderfully expressive hand-waving in support of Lamarckism. 
      He is ignoring the rachet effect.  I replied by quoting some
      stern mathematical proofs (from Nilssen and Pelger 1994) to show
      the probability of an eye evolving is not, in fact, infinitesimal,
      but odds-on, given the rachet.  Going back to Gallic
      hand-waving is no way to pursue this argument, and I see no need
      to comment further.

      HJP: The maths is so ludicrous

      DR: I’m happy to examine the maths with you, but you seem to be
      rejecting it on the basis of its conclusions, not its assumptions
      or working out of its steps.  That really is ludicrous
      (playing games).  You really have to engage with the
      argument: which assumption is wrong? which step is mistaken? 
      All you are doing is telling me that the conclusions contradict
      your intuitions. So much the worse for your intuitions. 
      Intuition is not your friend when it comes to statistics. 
      Crick’s book talks about ‘an inherent failure of the human mind
      when confronted with probability arguments’. 

      HJP: (And i am afraid that your adding in your last P.S
      that we “do know the random mutation rate for the genes in
      question…” is, I am sorry, absurd.)

      DR: I quoted you the Martinez/Baquero review of the scientific
      studies which describe the immense amount we now know about mutation
      rates in bacteria.  I see you are a man not easily swayed by
      proof.

      Speciation

      HJP: The diversity of the plant and animal kingdoms
      came about by no more than freak doubling of DNA-sometimes all of
      it?
      Be reasonable, please.

      DR: Not all of the diversity, just some of it. 
      Reasonableness, in accepting polyploidy as an occasional mechanism
      of speciation, is just what I am asking for.  [Polyploidy
      also explains another point that you once seemed to think counts
      against neo-Darwinism, namely that goldfish have a greater number
      of chromosomes than do humans.] 

      HJP: And when did Dobzhansky abandon the Strong Species
      Definition, please?

      DR: By 1977, at least.  I have here my old hardback copy of
      Evolution, by Dobzhansky et al., published in 1977,
      where they discuss species and speciation in less rigid terms
      throughout Chapters 5, 6 and 7, giving several different
      approaches to definition as appropriate to the groups being
      discussed.  [Do note that, regardless of his change of mind,
      I think no practising biologist is using his 1937 definition
      today, and I don’t even know how many would go along with all of
      his 1977 discussion.]

      HJP: To argue that Boxhorn´s stuff “could” be leading to
      speciation is all very well.
      But the FAQ is headed
      Observed Instances Of Speciation, is it not?

      DR: I would prefer to focus on the substance of the argument, if
      we are going to go over this again.  The examples are (a)
      pretty damn close by Dobzhansky’s 1937 definition, and (b) well
      over the goal line by any modern definition.

      Miscellaneous

      HJP: 5) Useful Mutations Never Happen
      Two observations re the initial stuff you posted re claism of
      observed favourable mutation in bacteria:
      First “The database is currently undergoing restructuring and data
      valuation” so the claimed evidence is not in fact available.

      DR: I don’t know where you got that phrase from.  (Not from
      anything I’ve pointed you to, I think, although you may have
      picked something up from another Tweeter.  I Googled that
      phrase and couldn’t find it anywhere.)  Be that as it may,
      the Martinez/Baquero paper links to shedloads of evidence.

      HJP: Second, the only experiment that could, without
      doubt, prove mutation in response to antibiotics is a physical and
      logical impossibility. The “evidence” claimed is in fact an
      inference not empirically determined as claimed.

      DR: You keep making this mistake.  The “impossibility” is
      only in Milton’s mistaken fantasy of how the experiments might
      have been conducted.  Meanwhile, using the correct
      experimental technique, it’s been proven over and over
      again.  The number of papers is immense, and some are linked
      in that Martinez/Baquero paper, and some of the papers have the
      full text available. 

      HJP: You cite the darkened type of Peppered Moth as an
      example of a mutation sometimes proving useful.
      But you have no idea how it darkened in the first place.
      How do you know any mutation ever caused that?
      An assumption.
      Rational enough certainly. But still an assumption.

      DR: Ah, sorry, quite right.  I can’t imagine how else
      variation arises in species, not being a member of the school of A
      Big Boy Did It And Ran Away.  Nonetheless, there is a deal of
      evidence supporting the assumption of a single original melanic
      mutation in these moths.  Discovering the genetic basis of a
      mutation is not a quick or a simple matter in complex organisms,
      but see van t’Hoff’s paper http://www.sciencemag.org/content/332/6032/958.full

      which strongly suggests that a mutation in a single individual
      gave rise to the melanic form.  Still, there are enough
      bacterial examples not to insist on the point.

      HJP: 6) Complex Life cycles
      (…)
      And Halipegus´ life cycle sits comfortably with the gradual
      assimilation, over millions of years, of useful accidental
      changes, eh?

      DR: Handwaving. Why couldn’t it have appeared by natural
      selection? This is the Argument from Lack of Imagination again. 
      The person who discovered the unusual fourth host stage explains
      how this life-cycle, when compared with the life-cycles of
      closely-related species, shows evolutionary adaptation to its
      environment.

      HJP: 7) Convergent evolution: Doppelgangers
      For many of us the appearance in isolated environs of the same
      thing – only difference is reproductive system -is amongst the
      strongest possible evidence that natural selection of spontaneous
      mutations is not what wrought the forms and also amongst the
      strongest possible evidence that some other unknown process or
      processes must have been involved.

      DR: You keep stating that as a conclusion without developing it
      as an argument.  You quote Coyne at length without explaining
      why he is wrong.  Why couldn’t similar forms (not the ‘same
      thing’) have appeared by natural selection?  Placental moles,
      mole rats, marsupial moles, golden moles… they share some common
      external adaptations because they have a common burrowing
      lifestyle, but they are all rather different inside and out. 
      I’m no more surprised by their similar features than I am by the
      fact that sharks, crocodiles and dolphins all have pointed snouts
      with sharp teeth.  ‘Gliding’ in frogs seems to have evolved
      30 times.  Or are all these Doppelgangers too? 
      Convergence is more of an argument for evolution than for …
      whatever it is that you believe.

      And you (and Coyne) gloss over many differences between say, the
      placental wolf and the marsupial ‘wolf’ (Thylacine or Tasmanian
      Tiger).  The rough bodily outline of the marsupial is
      similar, but the feet are too big, the front legs are relatively
      short, the skull is all wrong (having more in common with a
      kangaroo’s), and so on.  It would have been rather an
      ungainly animal, although apparently it was capable of a
      “shambling canter”.  It’s jaw had a very wide gape, and its
      canine teeth had an oval cross-section, strong enough to crush a
      skull; placental wolves have narrow canines used to slash. 
      They are rather different animals, given anything more than a
      passing glance.  Not the same thing at all.

      [And you are mistaken in claiming that the only difference
      between placentals and marsupials is how they reproduce. 
      Marsupials share a whole set of features (http://austhrutime.com/marsupial_vs_placental.htm,
      http://www.nhc.ed.ac.uk/index.php?page=493.168.257)
      besides their reproductive habits – common features that are
      explained most plausibly by their common evolutionary ancestry.]

      HJP: Right.
      You seem to have colossal optimism that every now and again a
      change for the better will be dished up via spontaneous mutation.
      This confidence we do not share.
      It´s wishful thinking, not observation.

      DR: You keep saying there are no observations, and when I point
      you to the observations, you say they are not there.  (“I see
      no ships”?)  We know mutations happen, we have a fair idea of
      with what frequency they appear, and any proposed mechanism for
      evolution by natural selection which gets to the point of
      testability is put on the rack of mathematical modelling to see if
      it breaks.  Nilssen and Pelger show it’s theoretically
      possible, even for the eye, and Lenski shows that it happens in
      practice, the Martinez paper lists loads of examples… It’s a lot
      more than wishful thinking.

      HJP: Would you care to comment on the absence of
      transitional fossils in the Antipodes for these mirror images, Dr?

      DR: I do wish you wouldn’t keep raising new
      distractions.   Nonetheless, within a minute, I found
      this:

      http://www.ncbi.nlm.nih.gov/pubmed/21047857 
      Even if I couldn’t find anything, the patchiness of the fossil
      record is no embarrassment to Darwinism, of course.  And I
      fear, even if the record for all marsupials was as complete as for
      some placentals, would you accept it as good evidence for
      evolution?  Where we do find transitional fossils, like those
      for whales or horses, do you accept them as evidence for
      evolution? I fear I can guess the answer.

      8) Natural selection too slow
      HJP: That was not the point of Crick and Milton.

      Sorry, I misunderstood the point.  See above.

      There are other points you made which I don’t
      understand/appreciate and haven’t addressed, often raising new
      issues.  If there’s one you feel is a cruncher, then of
      course I will reconsider it, but I really don’t want to keep
      addressing new points without feeling we have at least identified
      the points of difference among the issues already raised. 

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