Does Basener and Sanford’s model of mutation versus selection show that deleterious mutations are unstoppable?

by Joe Felsenstein and Michael Lynch

The blogs of creationists and advocates of ID have been abuzz lately about exciting new work by William Basener and John Sanford. In a peer-reviewed paper at Journal of Mathematical Biology, they have presented a mathematical model of mutation and natural selection in a haploid population, and they find in one realistic case that natural selection is unable to prevent the continual decline of fitness. This is presented as correcting R.A. Fisher’s 1930 “Fundamental Theorem of Natural Selection”, which they argue is the basis for all subsequent theory in population genetics. The blog postings on that will be found here, here, here, here, here, here, and here.

One of us (JF) has argued at The Skeptical Zone that they have misread the literature on population genetics. The theory of mutation and natural selection developed during the 1920s, was relatively fully developed before Fisher’s 1930 book. Fisher’s FTNS has been difficult to understand, and subsequent work has not depended on it. But that still leaves us with the issue of whether the B and S simulations show some startling behavior, with deleterious mutations seemingly unable to be prevented from continually rising in frequency. Let’s take a closer look at their simulations.

Basener and Sanford show equations, mostly mostly taken from a paper by Claus Wilke, for changes in genotype frequencies in a haploid, asexual species experiencing mutation and natural selection. They keep track of the distribution of the values of fitness on a continuous scale time scale. Genotypes at different values of the fitness scale have different birth rates. There is a distribution of fitness effects of mutations, as displacements on the fitness scale. An important detail is that the genotypes are haploid and asexual — they have no recombination, so they do not mate.

After giving the equations for this model, they present runs of a simulation program. In some runs with distributions of mutations that show equal numbers of beneficial and deleterious mutations all goes as expected — the genetic variance in the population rises, and as it does the mean fitness rises more and more. But in their final case, which they argue is more realistic, there are mostly deleterious mutations. The startling outcome in the simulation in that case is there absence of an equilibrium between mutation and selection. Instead the deleterious mutations go to fixation in the population, and the mean fitness of the population steadily declines.

Why does that happen? For deleterious mutations in large populations, we typically see them come to a low equilibrium frequency reflecting a balance between mutation and selection. But they’re not doing that at high mutation rates!

The key is the absence of recombination in these clonally-reproducing haploid organisms. In effect each haploid organism is passed on whole, as if it were a copy of a single gene. So the frequencies of the mutant alleles should reflect the balance between the selection coefficient against the mutant (which is said to be near 0.001 in their simulation) versus the mutation rate. But they have one mutation per generation per haploid individual. Thus the mutation rate is, in effect, 1000 times the selection coefficient against the mutant allele. The selection coefficient of 0.001 means about a 0.1% decline in the frequency of a deleterious allele per generation, which is overwhelmed when one new mutant per individual comes in each generation.

In the usual calculations of the balance between mutation and selection, the mutation rate is smaller than the selection coefficient against the mutant. With (say) 20,000 loci (genes) the mutation rate per locus would be 1/20,000 = 0.00005. That would predict an equilibrium frequency near 0.00005/0.001, or 0.05, at each locus. But if the mutation rate were 1, we predict no equilibrium, but rather that the mutant allele is driven to fixation because the selection is too weak to counteract that large a rate of mutation. So there is really nothing new here. In fact 91 years ago J.B.S. Haldane, in his 1927 paper on the balance between selection and mutation, wrote that “To sum up, if selection acts against mutation, it is ineffective provided that the rate of mutation is greater than the coefficient of selection.”

If Basener and Sanford’s simulation allowed recombination between the genes, the outcome would be very different — there would be an equilibrium gene frequency at each locus, with no tendency of the mutant alleles at the individual loci to rise to fixation.

If selection acted individually at each locus, with growth rates for each haploid genotype being added across loci, a similar result would be expected, even without recombination. But in the Basener/Stanford simulation the fitnesses do not add — instead they generate linkage disequilibrium, in this case negative associations that leave us with selection at the different loci opposing each other. Add in recombination, and there would be a dramatically different, and much more conventional, result.

Technical Oddities

Most readers may want to stop there. We add this section for those more familiar with population genetics theory, simply to point out some mysteries connected with the Basener/Stanford simulations:

1. One odd assumption that they make is that any fitness class that has a frequency below 1 part in a billion gets set to 0. This is not a reasonable way to take genetic drift into account, as all fitness classes are subject to random fluctuations. We imagine such a treatment is a minor issue, relative to the enormous mutation pressure imposed in their study. But someone should check this, which can be done as their Javascript source can be downloaded and then made comprehensible by a Javascript beautifier.

2. The behavior of their iterations in some cases is, well, weird. In the crucial final simulation, the genetic variance of fitness rises, reaches a limit, bounces sharply off it, and from then on decreases. We’re not sure why, and suspect a program bug, which we haven’t noticed. We have found that if we run the simulation for many more generations, such odd bouncings of the mean and variance off of upper and lower limits are ultimately seen. We don’t think that this has much to do with mutation overwhelming selection, though.

3. We note one mistake in the Basener and Sanford work. The organisms’ death rates are 0.1 per time step. That would suggest a generation time of about 10 time steps. But Basener and Stanford take there to be one generation per unit of time. That is incorrect. However the mutation rate and the selection coefficient are still 1 and 0.001 per generation, even if the generations are 10 units of time.

Joe Felsenstein, originally trained as a theoretical population geneticist, is an evolutionary biologist who is Professor Emeritus in the Department of Genome Sciences and the Department of Biology at the University of Washington, Seattle. He is the author of the books “Inferring Phylogenies” and “Theoretical Evolutionary Genetics”. He frequently posts and comments here.

and

Michael Lynch is the director of the Biodesign Center for Mechanisms of Evolution at Arizona State University, and author of “The Origins of Genome Architecture” and, with Bruce Walsh, of “Genetics and Analysis of Quantitative Traits”. Six of his papers are cited in the Basener/Stanford paper.

318 thoughts on “Does Basener and Sanford’s model of mutation versus selection show that deleterious mutations are unstoppable?

  1. Behe:

    If some peculiar feature is shared between two species which, as far as we can tell, has no particular function, and which in other contexts we would likely call a genetic accident, then I count that as rather strong evidence for common descent.

    Behe:

    “Both humans and chimps have a broken [non-functional] copy of a gene that in other mammals helps make vitamin C. … It’s hard to imagine how there could be stronger evidence for common ancestry of chimps and humans. … [additional] compelling evidence for the shared ancestry of humans and other primates comes from… a broken hemoglobin gene. … If a common ancestor first sustained the mutational mistakes and subsequently gave rise to those two modern species, that would very readily account for why both species have them now.”

    The Edge of Evolution, pages 71-72.

  2. colewd: So you are claiming once chromosome structure emerges in a population then splicing automatically emerges?

    No, those are words you’ve invented and put in some else’s mouth so that you can point to how absurd they are. It’s clear that what’s absurd is your understanding of what is claimed because it seems that you genuinely believe that what you are saying is what people are actually claiming despite the fact you can’t provide a single citation.

    colewd: No need to link anything unless it explains the origin of the sequences. The “just so” stories are not real explanations.

    You seem to have confused how science works with your fairy stories. Calling an explanation “not real” is just a way of dodging the accumulated evidence.

    The point is when we compare and contrast the “just so” explanations I have provided with your literal “just so – the designer did it” it’s clear that the ones I have provided are significantly more data rich then your version.

    colewd: I am pointing out that no one has a detailed explanation for life’s diversity.

    Well, Darwin had a fairly detailed explanation. But it all hinges on how detailed you mean. Obviously for you nothing short of a video tape will suffice, but of course you don’t apply the same restriction to your beliefs about intelligent design. On the basis of literally nothing you prefer ID over science.

    colewd: The problem is science making unsupported claims. The good news is that I see the claims becoming more realistic at this point.

    It’s nice that you admit your claims regarding Intelligent Design are not science, given that you have also admitted those claims are without support.

    colewd: I think the attempts to separate mechanism (natural selection etc) from common descent shows that some evolutionary biologists are backing off Darwin’s claims.

    What does that even mean. Citation please.

    colewd: Behe appears to be making progress with his argument supporting common descent but requiring design for new innovation.

    It seems you define “progress” in a similar way to that which you define “detail”. What “progress” has Behe made lately? Be specific.

  3. colewd: In order to form a functional 1300 AA protein many things need to happen together. The probability of event A (1300 AA functional protein forming) requires other events B,C,D happening together or P of A = P of AxBxCxD. To translate this protein you need to have formed through the evolutionary process:
    -chromosome in the correct state

    What is a “chromosome state”?

    -the proper intron splicing site codes

    Why does it need to have introns? Why can’t it simply form without introns?

    -exons that merge into a functional protein
    -exon sequences that merge into a functional sequence

    Those two are the same, and are entailed by it having “proper intron splicing site codes”. But why would it need to have introns? Why can’t it simply be an intron-free gene?

    -the proper start and stop condons

    Sure, but those are basically just part of there being a translatable region.

    -a transcription protein complex that binds to the DNA sequence

    Transcription factors and regulatory proteins already exist in living organisms, they don’t have to evolve de novo for every new protein. All a novel protein coding gene needs here is a binding spot to initiate transcription by already existing and active regulatory proteins.

    But as we already know (in part thanks to the ENCODE project), basically the entire genome is transcribed at a low noisy level. This is enough for natural selection to enhance should one of those noise-level transcripts prove functional in a beneficial way.

    In fact, that’s how comparative genetics has revealed de novo proteins usually evolve.

    -all the above for the transcription proteins in the protein complex

    What protein complex? Are you just typing stuff to make your list appear bigger than it needs to be? That’s what i looks like.

    -the code in order for the sequence to pass through the nuclear pore complex

    What code is that?

  4. Rumraket: Are you just typing stuff to make your list appear bigger than it needs to be?

    it seems their argument boils down to the 747 forming from a tornado in a junkyard.

    I’ve asked colewd to provide a citation for someone who is trying to solve the problem of first life and who is also assuming that it’s the same as extant life but so far he’s been unable to provide such. But I’ll keep asking just as sure as he will keep pretending to miss it.

  5. OMagain: it seems their argument boils down to the 747 forming from a tornado in a junkyard.

    Yep, always the same. It all has to happen in a single event, it can’t happen gradually under natural selection.

  6. colewd:

    Behe appears to be making progress with his argument supporting common descent but requiring design for new innovation.

    What is his “argument”? I’ve never seen an argument from him that didn’t just assume design rather than actually demonstrate it.

    I like a recent claim by KF that genetic engineering indicates that design can occur in life. Yes, do you know how we can discover that design has occurred in life? Because it stands out so strongly against the background of evolutionary limitations, you know, those facts that you won’t properly face.

    That’s how you know design has occurred–you see in life the signs of intelligence that doesn’t adhere to the limits of evolution. What don’t you have? Any evidence like that. Just your blithering on and on about anything that you can find that isn’t well-explained by evolution as yet, while you provide no meaningful explanations at all. Least of all, evidence that explains why, say, bird wings are fused out of bones that became articulated in their ancestors (and spare me that idiotic non-answer that flight has to be designed, it’s disgusting that you never will face up to the evidence).

    You can’t explain anything that evolution does, let alone anything it doesn’t.

    Glen Davidson

  7. Rumraket,

    Yep, always the same. It all has to happen in a single event, it can’t happen gradually under natural selection.

    It can happen any time during evolutionary history but it has to happen at some point for the protein we observe to form.

  8. colewd: It can happen any time during evolutionary history but it has to happen at some point for the protein we observe to form.

    No, the point is there is no “it”. There are lots of small “its”.

  9. colewd: Why don’t we start with a bicycle

    Why don’t you start with an honest appraisal of the existing evidence and join that to asking real questions grounded in what that evidence is attempting to explain. Not “atoms are designed”. You can believe whatever you like as far as religion goes (and that is religion) but few are really interested in exploring those beliefs. Your claims regarding your misunderstanding of evolution you can be educated on those. Or at least have why you are wrong explained to you in such detail that you might think twice before repeating the same strawman mischaracterization, some twinge of doubt or guilt perhaps.

    smiley face.

  10. colewd: It can happen any time during evolutionary history but it has to happen at some point for the protein we observe to form.

    Why don’t we observe your purported designer making changes in real time? Did your designer intervene in the LTEE? If so, when and how do you know? Why?

  11. Rumraket,

    What is a “chromosome state”?

    Where the chromosome is available for some function i.e. cell division or transcription.

    Why does it need to have introns? Why can’t it simply form without introns?

    For gene expression timing in embryo development and additional protein isoforms through alternative splicing.

    But as we already know (in part thanks to the ENCODE project), basically the entire genome is transcribed at a low noisy level. This is enough for natural selection to enhance should one of those noise-level transcripts prove functional in a beneficial way.

    Genes that look like noise in a developed animal can be highly expressed during embryo development. The WNT pathway is an example.

    What protein complex? Are you just typing stuff to make your list appear bigger than it needs to be? That’s what i looks like.

    A group of individually translated proteins that bind together to form a function. Transcription factors are an example.

  12. OMagain,

    No, those are words you’ve invented and put in some else’s mouth so that you can point to how absurd they are. It’s clear that what’s absurd is your understanding of what is claimed because it seems that you genuinely believe that what you are saying is what people are actually claiming despite the fact you can’t provide a single citation.

    If you think Adapta has a legitimate claim then you can explain it.

  13. OMagain,

    Why don’t we observe your purported designer making changes in real time? Did your designer intervene in the LTEE? If so, when and how do you know? Why?

    If the designer had intervened wouldn’t you expect at least a frog to evolve 🙂

  14. OMagain,

    Why don’t you start with an honest appraisal of the existing evidence and join that to asking real questions grounded in what that evidence is attempting to explain. Not “atoms are designed”.

    What is your explanation for the specificity and repeatability of atoms?

  15. OMagain,

    No, the point is there is no “it”. There are lots of small “its”.

    During evolutionary history you have less than 10^50 its available. You have lots of trial and error its required to express a functional protein of 1300 AA.

  16. Adapa: Or at least a Creationist with a brain.

    Or one with the guts to say “I don’t know my if proposed designer intervened during the LTEE to change the direction of evolution of the bacteria”. They want to have it all the ways, make strong claims (evolution cannot do anything of substance) but then refuse to comment when evolution is demonstrated to do something of substance in a lab in a traceable way and instead try to use lame “humour” to deflect from their utter lack of integrity.

    smileyface

  17. colewd:
    OMagain,

    During evolutionary history you have less than 10^50 its available.You have lots of trial and error its required to express a functional protein of 1300 AA.

    Still making the same dumb mistake, assuming the protein had to fall together all at once instead of evolving gradually through a feedback process with selection and inheritance involving small incremental changes from simpler yet functional precursors.

    Do you know how to play poker?

    Dealing 5 cards at random from a 52 card deck the probability of getting a royal straight flush are a bit better than 1 in 650,000. On average once every 650,000 deals you’d get a RSF.

    However now if you add selection feedback and inheritance where you are allowed to discard and redraw as many times as you want, keeping beneficial cards each time, you can virtually always accumulate a royal straight flush in less than a few dozen deals.

    Evolution has “discarding and redrawing” for around 4 billion years.

  18. OMagain: Or one with the guts to say “I don’t know my if proposed designer intervened during the LTEE to change the direction of evolution of the bacteria”. They want to have it all the ways, make strong claims (evolution cannot do anything of substance) but then refuse to comment when evolution is demonstrated to do something of substance in a lab in a traceable way and instead try to use lame “humour” to deflect from their utter lack of integrity.

    smileyface

    You notice none of them will ever comment on Behe’s claim the Intelligent Designer directly intervened to give malaria a resistance to new anti-malarial drugs. That makes their Designer God a rather sadistic bastard who still has it out for humans.

  19. OMagain,

    Dealing 5 cards at random from a 52 card deck the probability of getting a royal straight flush are a bit better than 1 in 650,000. On average once every 650,000 deals you’d get a RSF.

    However now if you add selection feedback and inheritance where you are allowed to discard and redraw as many times as you want, keeping beneficial cards each time, you can virtually always accumulate a royal straight flush in less than a few dozen deals.

    Evolution has “discarding and redrawing” for around 4 billion years.

    Do you believe that Adapta just described evolution accurately with the above analogy?

  20. OMagain: it seems their argument boils down to the 747 forming from a tornado in a junkyard.

    colewd: it seems their argument boils down to the 747 forming from a tornado in a junkyard.

    Why don’t we start with a bicycle

    Better still, why not start with how that tornado showed up?

    That tornadoes can occur naturally, already refutes what you seem to be arguing.

  21. colewd:
    Rumraket,

    Where the chromosome is available for some function i.e. cell division or transcription.

    The chromosomes are always “available for some function”. What you’re saying is nonsensical. It’s like saying you can only walk when “your legs are available for standing on”. Right, when are they not? Again, the fact that the majority of the genome is transcribed at low levels in basically all tissues demonstrates that all the chromosomes are “available” for transcription.

    For gene expression timing in embryo development and additional protein isoforms through alternative splicing.

    I’m aware that introns can contribute to functions of genes, but there are also genes that function without them. Why is it a requirement that all gene has introns? That can’t be the case, since we know of genes without them. You are also aware that most introns are thought to be selfish (in the sense of quasi-parasitic) junk-DNA right?

    Genes that look like noise in a developed animal can be highly expressed during embryo development.The WNT pathway is an example.

    Thank you for that irrelevant statement. That fact is not in question. I was explaining to you that transcription of all DNA at the level of noise is an inherent property of the transcription machinery. As such, any particular stretch of DNA has the potential to be iteratively honed by natural selection into a more actively transcribed stretch of DNA.

    A group of individually translated proteins that bind together to form a function.Transcription factors are an example.

    Why is that a requirement for a given arbitrary protein coding gene? The fact that many proteins work together in large complexes does not mean that for a functional gene to arise, it has to participate in such a manner.

    It looks to me like you just tried to add all the constraints you could think of to make it appear like there are more factors constraining protein evolution. You are mistaking specific cases for the general case, by making it appear as if these factors are necessary conditions for functional all functional genes.

  22. colewd:
    OMagain,

    Do you believe that Adapta just described evolution accurately with the above analogy?

    Did you even understand it? Do you finally understand why your “it’s too improbable” argument is so worthless?

  23. colewd: What is your explanation for the specificity and repeatability of atoms?

    The same basic physical forces are in operation everywhere in the cosmos.

    What is yours, and how do you know?

  24. colewd: During evolutionary history you have less than 10^50 its available. You have lots of trial and error its required to express a functional protein of 1300 AA.

    And where is the problem?

  25. colewd: Do you believe that Adapta just described evolution accurately with the above analogy?

    It is accurate enough to get across the principle of natural selection. Rather than having to keep drawing full decks on by one and discard any deck that is off even by a single card, in serial fashion, until you hit a perfect fit, with natural selection you can build up the deck slowly from a more randomized deck if it has a little bit of functionality, even if it doesn’t look exactly like the full deck.

  26. colewd: Are you equating the function of a tornado to a living organism?

    No, the problem is that you are equating the function of a tornado to evolution by natural selection!

    Where in the tornado does the selection aspect factor in? Where does incremental copying with mutations factor in? Nowhere. So the tornado analogy unavoidably fails as a proper analogy for evolutionary processes that involve selection.

  27. colewd: I am inferring creation based on argument from analogy.

    Analogy to what?

    Atoms are the same everywhere in the universe, therefore they were created. Uhm, why? I’m missing some sort of “analogy” that explains how that conclusion follows. Please enlighten us.

  28. Rumraket,

    Atoms are the same everywhere in the universe, therefore they were created. Uhm, why? I’m missing some sort of “analogy” that explains how that conclusion follows. Please enlighten us.

    Lets table this to a different thread.

  29. Rumraket,

    Where in the tornado does the selection aspect factor in?

    When a 747 appears it is selected for as an analogy. For selection to occur you need advantageous function that will aid in reproduction. Selection only fixes a feature in the population if that feature provides a reproductive advantage. Start with trying to explain the origin of transcription factors.

  30. colewd: Selection only fixes a feature in the population if that feature provides a reproductive advantage.

    But reproductive advantage is not necessary for a feature to be fixed in a population. Right?

  31. As somebody who mostly lurks here, I must say that it’s quite unfortunate that the discussion of this interesting OP has developed, like always, into debates about the same old nonsense.

    This current conversion could almost literally take place in any thread here. Just sayin’.

  32. I joined this group in part because I was under the impression this was the place where the smarter creationists hang out. But who do I find? Folks like J-Mac, Robert Byers and Bill Cole. Oh well.

  33. colewd: Do you believe that Adapta just described evolution accurately with the above analogy?

    No, Adapa has demonstrated that your ID-math(tm) P(A&B&D) = P(A)xP(B)xP(D) assumes independent events and is thus hopelessly wrong.
    Personally, I like Levinthal’s paradox: since there are over 10^123 possible configurations of cholera toxin’s B chain, therefore, according to ID-math(tm), the designer must step in to help each molecule fold. That’s one industrious and malevolent designer you got there, mate.

  34. Dave Carlson:
    As somebody who mostly lurks here, I must say that it’s quite unfortunate that the discussion of this interesting OP has developed, like always, into debates about the same old nonsense.

    This current conversion could almost literally take place in any thread here.Just sayin’.

    Ok, something substantive….

    Dave, one interesting point if you run the java script simulation, it confirms Ewens and Lessard’s claim that Fisher’s forumula doesn’t predict long term direction, but it does predict the connection of variance and rate of fitness change.

    Run Basener’s simulation, it’s EASY!:
    https://people.rit.edu/wfbsma/evolutionary%20dynamics/EvolutionaryModel.html

    This is Fisher’s theorem:

    “The rate of increase in fitness of any organism at any time is equal to its genetic variance in fitness at that time.”[3]

    Note the graphs in Basener’s simulation of “rate of increase of fitness” and “variance in fitness”. The two graphs are identical!! Just as Fisher predicted! However, note that fitness can still decline as Ewens and Lessard predicted.

    I think the OP has misread and over-interpolated some of what was said in Basener’s paper.

  35. colewd: When a 747 appears it is selected for as an analogy.

    What the fuck does that even mean? In what way is the appearance of a tornado like natural selection among different carriers of mutations?

    For selection to occur you need advantageous function that will aid in reproduction.

    Yes. How does a tornado accomplish that?

    Selection only fixes a feature in the population if that feature provides a reproductive advantage.

    Selection increases the rate of fixation, but even neutral or deleterious mutations can be fixed. I’m still not clear on what any of this has to do with your terrible tornado-analogy.

    A tornado appears and randomly throws stuff around in piles. Where is natural selection happening here? What is a “mutation” in this analogy? Where does reproduction take place?

    Start with trying to explain the origin of transcription factors.

    All of that has been done to death a thousand times. But you’re still stuck on this terrible tornado analogy that has basically nothing to do with evolution by natural selection.

  36. DNA_Jock,

    No, Adapa has demonstrated that your ID-math(tm) P(A&B&D) = P(A)xP(B)xP(D) assumes independent events and is thus hopelessly wrong.

    Are you claiming that all the origin of all the processes that lead to the translation of a 1300 AA protein are not independent? Can you support this claim, mate?

  37. stcordova: I think the OP has misread and over-interpolated some of what was said in Basener’s paper.

    Sooo, you’ll be busy over the next couple months trying to explain on various pro-ID and creationist blogs how Basener and Sanford’s new paper don’t actually show what they take it to say on all those various websites, right?

    You’ll be busy explaining how all it shows is that under some particular set of conditions, natural selection can’t get rid of all deleterious mutations leading to fitness delcine, but this isn’t actually a problem for our current understanding of the evolutionary history of life, nor is it some inherent flaw that invalidates natural selection, nor do those conditions necessarily always, or even mostly obtain in the real world. Right?

    You’ll be busy telling all the IDcreationists that all Basener and Sanford shows is that under some particular set of conditions, overall fitness can still decline, but population geneticists already knew this and don’t think this is an issue. Right?

    By the way, why would Basener and Sanford even write a paper with a trivial conclusion all population geneticists agree with?

    Sorry Sal, not buying it. Their paper is a carefully designed propaganda-piece. Concocted to be quotable by non-experts with lots of grandiose but easily copy-pasted claims and conclusions. Basener and Sanford are out to give the appearance of having “debunked” evolution by natural selection, not merely to assert what everyone else already knew.

  38. colewd: Are you equating the function of a tornado to a living organism?

    No, of course not.

    However, both (tornado and organism) have lower entropy than their surroundings. Both have some degree of non-random organization. Both are self-sustaining using energy that they can pick up. However, the tornado is self-sustaining for a far shorter period of time.

    Your argument, all along, appears to have been that self-organized self-sustaining systems cannot occur naturally. Weather systems demonstrate otherwise.

  39. Rumraket,

    A tornado appears and randomly throws stuff around in piles. Where is natural selection happening here? What is a “mutation” in this analogy? Where does reproduction take place?

    The tornado analogy by Hoyle was for origin of life which is prior to cell division. The 747 analogy is the first cell.

  40. Neil Rickert,

    Your argument, all along, appears to have been that self-organized self-sustaining systems cannot occur naturally. Weather systems demonstrate otherwise.

    Thats not my argument.

    My argument is that we have not identified a natural mechanism that accounts for the functional information inside DNA.

  41. By the way, why would Basener and Sanford even write a paper with a trivial conclusion all population geneticists agree with?

    Basener is a mathematician. He showed an alternate proof of Fisher’s theorem from Wilke, not Price. That counts for something original!

    The conclusion isn’t trivial. If all species diversified from a haploid non-recombining genome, the result constrains the evolution of our supposed ancestors as far as mutation rate. If fitness declines in the specific case, then one must question, “why are we here.”

    They may be intending to generalize the result later. 🙂 I don’t think the finite model will be so favorable to recombination as Joe predicts. Why??

    Near neutrals are defined by s (selection coefficient)

    s = 1/(4Ne)

    Ne is the finite case. And note, s =0.001 is a mean, there is an associated deviation from the mean.

    Soooo, this will fail in the case of recombination. Need I remind everyone, this derivation that applies to recombining populations that was shown by Kumrua, Eyre-Walker, Keightley, Nachman, Crowell and (hehe me):

    http://www.creationevolutionuniversity.com/science/?p=22

    But in any case, let me point out again why I grew negative one aspect of pop gen, namely fitness:

    http://theskepticalzone.com/wp/defining-fitness/comment-page-5/#comment-212087

  42. colewd: Are you claiming that all the origin of all the processes that lead to the translation of a 1300 AA protein are not independent? Can you support this claim, mate?

    I suspect that you do not understand the mathematical meaning of the word “independent”, but I’ll play along:
    Yes, that is my claim. My support: all the events depend on carbon chemistry.
    I don’t think you understood your own question, chum.
    ETA N.B. your ID-math is wrong if any two of the events are not independent. “All” is a goalpost shift.

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