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. Adapa: Too afraid to answer the simplest questions about their claims.

    They know, presumably from previous experience, that attempting to actually have a debate never ends well for them.

  2. J-Mac: Are bacteria in LTEE any closer to anything other than bacteria?

    What baramin are bacteria in? Did god create bacteria? All of them? Out of interest, how many species of bacteria do you think there are?

  3. Adapa: ID-Creationists make lots of stupid claims but “mutations can only decrease information” is one of the dumbest.The simple reason is what any one mutation can do, another can undo.

    If AAC –>AAG is a loss of information then
    AAG–>AAC must be a gain of information by definition

    Such mutations are empirically observed in the real world.They are called back mutations or reverse mutations.

    I eagerly await J-Mac and Phoodoo’s snotty non-answers to this simple fact for their entertainment value.

  4. Adapa,

    IDists all seem to have trouble with this. I remember ericB and the N.E.C.R.O. thread fondly…
    As an organism moves away from an optimum, the distribution of fitness deltas is expected to shift somewhat. This is what I alluded to earlier.

  5. Adapa,

    If AAC –>AAG is a loss of information then
    AAG–>AAC must be a gain of information by definition

    Such mutations are empirically observed in the real world.They are called back mutations or reverse mutations.

    Solid argument in a world made of single amino acid proteins.

  6. colewd:
    Adapa,

    Solid argument in a world made of single amino acid proteins.

    Solid argument in any world. I notice you have no rebuttal argument. Are you claiming back mutations don’t happen?

  7. colewd:
    Adapa,

    Solid argument in a world made of single amino acid proteins.

    The size of the protein is irrelevant. If a change of an amino acid in a protein 4000 aa’s long is a “loss of information”, then the reverse is a gain. There is no way around this.

    There must, by logical necessity, be an equal number of possible gain and loss of information mutations. Every loss implies a gain if reversed. It can’t be any other way.

  8. colewd: Solid argument in a world made of single amino acid proteins.

    Did you know the mutation that causes sickle cell anemia is a single nucleotide substitution (A to T) in the codon for amino acid 6?

  9. Rumraket,

    The size of the protein is irrelevant. If a change of an amino acid in a protein 4000 aa’s long is a “loss of information”, then the reverse is a gain. There is no way around this.

    I agree with you that a gain of information is possible after a loss of information. If we have a 4000 amino acid protein with functional information from where did that functional information originate?

  10. OMagain,

    Did you know the mutation that causes sickle cell anemia is a single nucleotide substitution (A to T) in the codon for amino acid 6?

    Sure, but do you think this really strengthens your argument?

  11. I’m not actually arguing anything colewd. I’m demonstrating something. It seems everyone knows what that is except a select few….

  12. colewd: If we have a 4000 amino acid protein with functional information from where did that functional information originate?

    Same question to you. Given that I have an answer that’s at least partially supported by evidence and you have literally no evidence for your position at all what is it that stops you admitting that our current best guess at the origin of that information is not a god.

    Given two unlikely claims for the origin of “functional information”, god and an iterative process of selection, is it not wise to place your bets on the one that has tentative support in the physical universe rather then the one based on wishful thinking?

  13. colewd: If we have a 4000 amino acid protein with functional information from where did that functional information originate?

    As a starting point you need to demonstrate that there is functional information there at all.

    colewd: I agree with you that a gain of information is possible after a loss of information.

    Otherwise how can you be sure that there was actually a loss of information in the first place?

    Or, in other words, how do you determine that a given change is a loss rather then a gain of “functional information”.

    Perhaps some changes happen and there is no change in the “functional information”. Perhaps a single change causes a large change in the “functional information”. Perhaps it takes a critical mass of changes to cause a large change in the “functional information”. Perhaps it depends on the information itself what level of changes are required to cause what effect.

    All these unclear points could be clarified if you’d simply explain how you determined that there was functional information present in the first place.

    After all, there might have been a mix up at the lab and you’ve been sent the wrong sample. That’d be embarrassing, right? If it turned out you had literally no way to determine if the “functional information” increased, decreased or stayed the same. Very embarrassing.

  14. OMagain,

    I’m not actually arguing anything colewd. I’m demonstrating something.

    You’re demonstrating that single mutations can be delirious. If this is a single event in the history of life then it is not a big deal but you would then be silly for mentioning it. If it is common then is supports Sanford’s argument. Are you hoping for the Goldilocks scenario 🙂

  15. colewd:

    You’re demonstrating that single mutations can be delirious.

    Um, no. But you’re demonstrating that single commenters can be.

  16. colewd:
    Rumraket,

    I agree with you that a gain of information is possible after a loss of information.If we have a 4000 amino acid protein with functional information from where did that functional information originate?

    Mutations of course. There can’t be loss of information if that information was not first gained.

  17. OMagain,

    Given two unlikely claims for the origin of “functional information”, god and an iterative process of selection, is it not wise to place your bets on the one that has tentative support in the physical universe rather then the one based on wishful thinking?

    Wishful thinking is finding a 4000 nucleotide sequence that can translate into an amino acid sequence and find a viable fold and function from a sequence of nucleic acids generated by trial and error.

    As big of this problem is it dwarfs the fact that a functional sequence that lives inside 4^3.2billion possible arrangements can build a human being came from a series of trial and error changes.

    I find your circular reasoning (God is just to big a concept so he must not exist) driving you to accept the highly improbable from nature.

  18. colewd: I find your circular reasoning (God is just to big a concept so he must not exist) driving you to accept the highly improbable from nature.

    When you start from a 4000 nucleotide sequence then yes, it’s a very improbable thing. But nobody is making the claim that such a sequence arose de novo.

    Unless you can provide a citation to that effect?

    If you want to name a specific complex then I can go and do the same google search you can do in order to determine what is currently known about the evolutionary history of that artifact.

    Would you like to play that game?

    colewd: I find your circular reasoning (God is just to big a concept so he must not exist) driving you to accept the highly improbable from nature.

    Your desire to prove that god left fingerprints has caused you to build a strawman of misunderstanding. It seems that nobody but you can set it aflame and you are unwilling do to that.

    But it’s try and set fire to it anyway.

    Name a specific thing that you believe god has created de novo. We can make an OP about it and discover what we collectively know about it’s origin. Then we can see if you are willing to reassess your claim in light of that new knowledge.

  19. colewd: As big of this problem is it dwarfs the fact that a functional sequence that lives inside 4^3.2billion possible arrangements can build a human being came from a series of trial and error changes.

    The entire solution space is not explored, only adjacent nodes to what which is already functioning. Many adjacent nodes that embody slightly different physical configurations are functionally the same (or close enough) which is what allows such entities to explore the local space incrementally.

    Again, provide a citation that a ” 4000 nucleotide sequence ” appeared doing something useful with no precursors whatsoever then perhaps your argument might have some merit. But you seem to be arguing against evolution while forgetting about the, well, evolution part. Perhaps before then 4000 version we had a 3999 version. Or a 2000 version. Can you guess what happened to the 2000 version to make a 4000 version?

  20. OMagain,

    Again, provide a citation that a ” 4000 nucleotide sequence ” appeared doing something useful with no precursors whatsoever then perhaps your argument might have some merit. But you seem to be arguing against evolution while forgetting about the, well, evolution part. Perhaps before then 4000 version we had a 3999 version. Or a 2000 version. Can you guess what happened to the 2000 version to make a 4000 version?

    If you believe that life originated on its own then the 4000 nucleotide sequence came from a trial and error process over time. There is no getting away from this claim. Since I find this highly improbable and think there is substantial additional evidence that we live in a created universe, I think these sequences were most likely created and not the result of trial and error.

  21. colewd: Wishful thinking is finding a 4000 nucleotide sequence that can translate into an amino acid sequence and find a viable fold and function from a sequence of nucleic acids generated by trial and error.

    Followed by:

    colewd: I find your circular reasoning (God is just to big a concept so he must not exist) driving you to accept the highly improbable from nature.

    I’d actually say it’s more probable to find a 4000 length sequence de novo then a deity that creates universes but then has to constantly fiddle because it could not get it’s shit together sufficiently to make it operate stand alone.

  22. colewd: If you believe that life originated on its own then the 4000 nucleotide sequence came from a trial and error process over time.

    What secrets do you know about the origin of life that nobody else knows? What is this 4000 nucleotide sequence that had to be present at the origin of life? You know you are just making this up now, right?

    colewd: There is no getting away from this claim.

    For you, no, that’s because the only place that claim exists is inside your mind. You can’t get away from that.

    colewd: Since I find this highly improbable and think there is substantial additional evidence that we live in a created universe

    Yes, your misunderstandings about biology make some things highly improbable. For example, your belief that the modern cell was the first life, not something simpler. In that regard, yes, I’d also agree the origin of life is highly improbable as a naturalistic event.

    colewd: I think these sequences were most likely created and not the result of trial and error.

    What sequences? Name them! Link to them!

  23. colewd: If you believe that life originated on its own

    What’s your belief? That life did not originate on it’s own? Anything more, er, detailed then that available?

  24. OMagain,

    Again, provide a citation that a ” 4000 nucleotide sequence ” appeared doing something useful with no precursors whatsoever then perhaps your argument might have some merit. But you seem to be arguing against evolution while forgetting about the, well, evolution part. Perhaps before then 4000 version we had a 3999 version. Or a 2000 version. Can you guess what happened to the 2000 version to make a 4000 version?

    I find this just so story without merit but thats just me 🙂 The issue is that with a long sequence the chance is higher that a sequence will move away from function then toward it. This is a part of Sanford’s claim which I think is valid.

  25. OMagain,

    What’s your belief? That life did not originate on it’s own? Anything more, er, detailed then that available?

    I believe that life and its diversity is the result of intelligent creation. The details beyond this may be outside our grasp.

  26. colewd: I believe that life and its diversity is the result of intelligent creation. The details beyond this may be outside our grasp.

    You believe that, as I have demonstrated via your inability to provide citations, based on a foundation of misunderstandings.

    Name a specific component of life that you believe must have been designed or admit that you don’t actually want to hear the truth.

  27. OMagain,

    Yes, your misunderstandings about biology make some things highly improbable. For example, your belief that the modern cell was the first life, not something simpler. In that regard, yes, I’d also agree the origin of life is highly improbable as a naturalistic event.

    How about the origin of the first eukaryotic cell as a naturalistic event or the origin of the first respiration system as a naturalistic event?

  28. colewd: I find this just so story without merit but thats just me

    So it’s literally impossible for a sequence 3999 long to turn into a sequence 4000 long? That’s literally beyond the bounds of possibility in this universe? Is that really your claim?

    colewd: The issue is that with a long sequence the chance is higher that a sequence will move away from function then toward it.

    A higher chance is just that. A chance. If there is a higher chance that it will move away from function then, by your own words, there is a lower chance it will move towards function. Right or wrong?

    colewd: This is a part of Sanford’s claim which I think is valid.

    Am I disputing that there are many more ways to break something then to improve it? No. What I’m trying to get you to see is that even if we have a lower chance to move towards function that’s still a chance. And if we do move towards function and that function provides an advantage, however slight, then can you not see that that sequence will spread at a higher rate then less advantageous sequences?

    Your mistake is thinking that current life was first life. And it seems you are going to cling onto that life raft regardless, as otherwise you’ll be adrift, alone in an uncaring universe…..

  29. OMagain,

    Name a specific component of life that you believe must have been designed or admit that you don’t actually want to hear the truth.

    ATP Synthese.

  30. OMagain,

    Your mistake is thinking that current life was first life. And it seems you are going to cling onto that life raft regardless, as otherwise you’ll be adrift, alone in an uncaring universe…..

    Please support your claim that first did not look like current life. This is your speculation base on your materialistic bias.

  31. colewd: How about the origin of the first eukaryotic cell as a naturalistic event or the origin of the first respiration system as a naturalistic event?

    https://www.ncbi.nlm.nih.gov/pubmed/8639327
    http://onlinelibrary.wiley.com/doi/10.1111/j.1574-6976.1996.tb00235.x/abstract?
    https://blogs.scientificamerican.com/lab-rat/the-origin-of-breathing-how-bacteria-learnt-to-use-oxygen/

    I don’t expect any of this to convince you. You are beyond convincing, it seems. Given that there are physical and biological pathways that have been elucidated in those links you cannot but admit that there are plausible explanations that don’t depend on the hand of god reaching down from the heavens.

  32. colewd: Please support your claim that first did not look like current life. This is your speculation base on your materialistic bias.

  33. OMagain,

    I don’t expect any of this to convince you. You are beyond convincing, it seems. Given that there are physical and biological pathways that have been elucidated in those links you cannot but admit that there are plausible explanations that don’t depend on the hand of god reaching down from the heavens.

    The spliceosome requires the organization of greater the 100k nucleotides. Can you pull any evidence out of these papers that explains how this molecular machine originated? I realized you are committed to naturalism even though you agree the problems we have with an origin of life explanation. The arguments your are trying to support are very difficult.
    .

  34. OMagain,

    colewd: ATP Synthese.

    Here you go

    So where do see an explanation of the origin of the DNA sequences that code for the protein complex?

  35. OMagain:

    Is that what OMGain looks like? Why is his heart exposed? Is he opening his heart literally?
    I hope that’s not the open hear surgery advertising where he comes from…

  36. OMagain,

    So where do see an explanation of the origin of the DNA sequences that code for the protein complex?

    I addition you have the problem of how this multi protein complex functions without the rest of the electron transport chain. We have no evidence of life without the ability to manufacture ATP rapidly which is a function of the electron transport chain.

  37. OMagain,

    I don’t expect any of this to convince you. You are beyond convincing, it seems.

    It’s not your ability to convince it is the lack of evidence that supports a natural explanation for the diversity of life. With an easier argument you would do pretty well.

  38. colewd: Wishful thinking is finding a 4000 nucleotide sequence that can translate into an amino acid sequence and find a viable fold and function from a sequence of nucleic acids generated by trial and error.

    Why?

  39. colewd: The issue is that with a long sequence the chance is higher that a sequence will move away from function then toward it.

    Why?

    This is a part of Sanford’s claim

    Where? It might be what Sanford believes, but where has he shown this? Quite it.

  40. colewd: The spliceosome requires the organization of greater the 100k nucleotides. Can you pull any evidence out of these papers that explains how this molecular machine originated?

    Change the goalposts much? What is it you want to discuss the origin of?

    But there are lots of interesting things out there if you care to look on the origin of the spliceosome. Would you like me to link you to some? Whereas you, of course, can only repeat “I believe it was Intelligently Designed”. GIven that, that you can only say that phrase when you asked the same questions you are asking me, and given that I can point to many many things discussing answers to exactly the questions you are are asking, does the asymmetry never trouble you?

    I mean, what exactly is it that you are arguing? It seems to me to be the biological equivalent of Sal’s YEC. Utterly implausible, totally unsupported by any evidence, never mind consiliant evidence and yet adherents are totally implacable in their dedication.

    colewd: I realized you are committed to naturalism even though you agree the problems we have with an origin of life explanation.

    There are plenty of people who believe in god and who do fantastic science. Many many people. It’s not about a commitment to this or that. It’s about honesty.

    colewd: The arguments your are trying to support are very difficult.

    I’m not really trying to support an argument. The support is there if you care to look for the argument you think I’m making. I’m just saying, given you got nothing why don’t you accept that honest, decent people actually have something legitimate to say about the evolutionary origin of all the things you’ve mentioned. What are all those papers about if not parts of a larger narrative based on some kind of naturalistic evolution?

    colewd: So where do see an explanation of the origin of the DNA sequences that code for the protein complex?

    The current sequence but with the seventh codon swapped with the eighth.

    colewd: I addition you have the problem of how this multi protein complex functions without the rest of the electron transport chain.

    Why is it a problem for me but not for you? Was everything poofed into being in one instant, or did some stuff come first?

    colewd: We have no evidence of life without the ability to manufacture ATP rapidly which is a function of the electron transport chain.

    OK, so what should we now insert into the textbooks at this point according to you?
    Out of interest, how has pointing to specific things as evidence for Intelligent Design worked out in the long run? How many unknowns in biology or science have actually ended up with “god” being accepted as the answer? Just wondering. That there are things we don’t know does not mean god did it. It just means there are things we don’t (yet) know.

    colewd: It’s not your ability to convince it is the lack of evidence that supports a natural explanation for the diversity of life.

    A lack vs zero. Some vs none. You go with the none side, every time.

    colewd: With an easier argument you would do pretty well.

    It’s not an argument. It’s an acceptance of reality. Zero vs something. Ignorance vs bliss.

  41. Rumraket,

    Why?

    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
    -the proper intron splicing site codes
    -the proper start and stop condons
    -exons that merge into a functional protein
    -exon sequences that merge into a functional sequence
    -a transcription protein complex that binds to the DNA sequence
    -all the above for the transcription proteins in the protein complex
    -the code in order for the sequence to pass through the nuclear pore complex
    etc.

  42. colewd:
    Rumraket,

    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.

    How many times are you going to make the same stupid mistake? Your probability value is only correct if A,B,C,D, are all completely independent events. That is not the case when you have an iterative process with feedback from selection and heritability i.e evolution. Once you have A providing a selectable advantage the mutation spreads until the whole population has A. Then anyone in the population can get A,B not just the single lineage with the initial A. Once A,B provides an advantage it spreads and becomes the population baseline; everyone has A,B. Then to reach A,B,C anyone in the population can get C.

    All all Creationists so ignorant of basic biology? Dembski and Axe both made the same blunder when they calculated their bogus probabilities.

  43. OMagain,

    Change the goalposts much? What is it you want to discuss the origin of?

    But there are lots of interesting things out there if you care to look on the origin of the spliceosome. Would you like me to link you to some? Whereas you, of course, can only repeat “I believe it was Intelligently Designed”. Given that, that you can only say that phrase when you asked the same questions you are asking me, and given that I can point to many many things discussing answers to exactly the questions you are are asking, does the asymmetry never trouble you?

    I don’t think the goal posts are moved as the spliceosome is one of the saltation events required to explain the eukaryotic origin.

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

    I mean, what exactly is it that you are arguing? It seems to me to be the biological equivalent of Sal’s YEC. Utterly implausible, totally unsupported by any evidence, never mind consiliant evidence and yet adherents are totally implacable in their dedication.

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

    I’m just saying, given you got nothing why don’t you accept that honest, decent people actually have something legitimate to say about the evolutionary origin of all the things you’ve mentioned.

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

    OK, so what should we now insert into the textbooks at this point according to you?
    Out of interest, how has pointing to specific things as evidence for Intelligent Design worked out in the long run? How many unknowns in biology or science have actually ended up with “god” being accepted as the answer? Just wondering. That there are things we don’t know does not mean god did it. It just means there are things we don’t (yet) know.

    I think the attempts to separate mechanism (natural selection etc) from common descent shows that some evolutionary biologists are backing off Darwin’s claims. Behe appears to be making progress with his argument supporting common descent but requiring design for new innovation.

  44. colewd:
    OMagain,

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

    Science has an excellent explanation backed up with huge amounts of positive evidence. Just because IDiots demand infinite detail doesn’t mean science knows of no details.

    I think the attempts to separate mechanism (natural selection etc) from common descent shows that some evolutionary biologists are backing off Darwin’s claims.Behe appears to be making progress with his argument supporting common descent but requiring design for new innovation.

    Making progress with who? The handful of IDiots who still buy the anti-science trash books the DI churns out? Behe hasn’t convinced a single soul in the actual scientific community of his IDiot claims.

  45. Adapa,

    How many times are you going to make the same stupid mistake? Your probability value is only correct if A,B,C,D, are all completely independent events. That is not the case when you have an iterative process with feedback from selection and heritability i.e evolution. Once you have A providing a selectable advantage the mutation spreads until the whole population has A. Then anyone in the population can get A,B not just the single lineage with the initial A. Once A,B provides an advantage it spreads and becomes the population baseline; everyone has A,B.

    So you are claiming once chromosome structure emerges in a population then splicing automatically emerges? Or once start and stop condons emerge then 3 prime and 5 prime splice sites emerge?

    This is great why didn’t you mention this before 🙂

  46. colewd:

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

    Did you finally come to grips with the fact that Behe accepts common descent, Bill?

    That really threw you for a loop. It was hilarious to watch.

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