Intelligent Design

Branko Kozulic responds to Professor Moran

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This is a continuation of an earlier post, A short post on fixation, to which Professor Moran replied here. He has asked Dr. Kozulic to contact him directly; Dr. Kozulic is now answering that request as co-author of the present post. We asked Professor Moran to answer three questions relating to the fixation of neutral mutations. But before dealing with his answers, let’s confirm that both sides agree that the key point at issue here is the fixation of neutral mutations in the human lineage, subsequent to its divergence from the lineage leading to chimpanzees. In Professor Moran’s words:

In an attempt to show them that evolution CAN account for the differences between humans and chimps/bonobos, I wrote up a description of how Neutral Theory and random genetic drift produce genomes that differ by 22 million positions if we take the fossil evidence at face value and assume that chimps and humans last shared a common ancestor about 5 million years ago [Why are the human and chimpanzee/bonobo genomes so similar?].

The questions that Professor Moran didn’t answer

In a previous reply to a post by Torley, Professor Moran elaborated on the mutation rate determined in long-term experiments with E. coli. But in our view there has never been any dispute on this point. Indeed, in our post (April 5, 2014), we treated the quoted figure from that study of 35 mutations as fixed mutations (see below), in order to show that the fixation rate Professor Moran stated for the human population was over five orders of magnitude greater than for E. coli, and that this striking fact was in need of explanation. Our hope was that Professor Moran would start discussing population sizes, but unfortunately, that did not happen.

Then we quoted from a well-known textbook on population genetics, John Gillespie’s Population Genetics: A Concise Guide (Johns Hopkins University Press, Baltimore, second edition, 2004):

If 1/μ << N, the time scale of mutation is much less than drift, leading to a population with many unique alleles. If N << 1/μ, the time scale of drift is shorter, leading to a population devoid of variation. (2004, p. 31)

In the passage above, μ [mu] refers to the mutation rate and N to the population size. We then added:

Professor Moran is kindly requested to state whether he agrees with this statement, and if not, to provide some references to support his views.

Professor Moran responded:

As for the question, I can’t really answer it because I don’t know what John Gillespie means by the mutation rate (μ). If it’s 10-10 per bp per generation then 1/μ equals 1010, or 10 billion. There are very few population sizes that are larger than 10 billion. If Gillespie means something like 10-4 mutations per generation (E. coli) or 100 mutations per generation (Homo sapiens) then I agree with him, although it seems a bit silly to be talking about a population size of 1/100 (1/μ) in the case of humans.

Obviously, it would be very silly to speak of any population having a size of 0.01, and not just a human one! Thus it appears that Professor Moran realized that something was wrong with the mutation figure he was using, of 100 mutations per generation, but he did not bother to check what it was.

(Actually, Gillespie states on page 30 that “mutation rates are often small (10-5 to 10-10 depending on the context)”, so the mutation rate μ can only refer to the mutation rate per nucleotide (bp) per generation. But if μ is 10-10 per bp per generation then 1/μ equals 1010, or 10 billion. Since the effective human population size N was 10,000 or less during most of the Paleolithic era, it would follow that N << 1/μ, "leading to a population devoid of variation," as Gillespie states. This runs completely contrary to the scenario Professor Moran is proposing: he maintains that there was sufficient variation to fix 100 mutations in each generation, from five million years ago to the present.)

Quoting again from John Gillespie’s text, Population Genetics: A Concise Guide (Johns Hopkins University Press, Baltimore, second edition, 2004, page 54), in the passage below, Ne refers to the effective population size, μ to the mutation rate and v to the variance in the change:

Figure 2.9 illustrates the beta density for three values of 4Neμ for a symmetrical model with μ=v. Notice that if 4Neμ<1, the probability mass is concentrated near the boundaries. In this case we expect – in a probabilistic sense – to find the allele frequency near either zero or one. If 4Neu>1, the allele frequency piles up near its deterministic equilibrium value of one-half. In the former case genetic drift dominates mutation; in the latter case mutation dominates drift. When 4Neu = 1, we have the peculiar case where neither force has the upper hand.

If the numerical value of the mutation rate (μ) is 100 (or 133), as used by Professor Moran, the product 4Neμ is for all population sizes larger than 1. If so, two important cases of population genetics models, when 4Neμ = 1 and when 4Neμ<1, have impossibly high values for μ. With the only possibility left, 4Neμ>1, “the allele frequency piles up near its deterministic equilibrium value of one-half”, and “mutation dominates drift” in all cases. It appears impossible to avoid the conclusion that the mutation rate used by Professor Moran is much larger than the values commonly used in population genetics models. (Alternatively, if μ should really be 10-10, then 4Neμ<1, which would mean that genetic drift would dominate mutation in an effective population of, say, 10,000, which was the effective human population size for most of the Paleolithic.)

It is possible to express the mutation rate per nucleotide, per locus or per individual genome, as we noted in our previous post. Regarding the time units: the mutation rates quoted in the literature are usually rates per generation, rather than per year. The experimentally determined numerical values vary somewhat from study to study, but we will use the above-mentioned value for E. coli of about 1×10-10 (Lenski) as the mutation rate per nucleotide. Since a locus is typically taken to contain 1000 nucleotides, the mutation rate expressed per locus is therefore 1000 times higher (for a locus containing 768 nucleotides, Gillespie gives the value of 7.83 x 10-7 per locus, and 1 x 10-9 per nucleotide, on page 32). Finally, we can express the mutation rate per individual genome, which corresponds to about 100 for the human genome.

The crux of our dispute with Professor Moran, as agreed by both sides (see above) is the feasibility of 22 million neutral mutations being fixed in the human population, over a period of five million years. These mutations are nucleotide mutations. Professor Moran is kindly asked to answer the following two questions.

First, since we are talking about nucleotide mutations here, why doesn’t he apply the value for the mutation rate per nucleotide in his calculation?

Our second, related question is: since the dispute between us is not about the fixation rate of individual genomes(?), then why does he use the value for the mutation rate per individual genome?

Can Professor Moran provide a credible model to support his claims regarding fixation?

Spread of Homo sapiens (1, red), Neandertals (2, olive) and early hominids (3, green). During most of the Paleolithic, the effective human population size was approximately 10,000. Figures shown on the map refer to arrival dates, in years before the present – for example, humans arrived in Australia 50,000 years ago and in Alaska 15,000 years ago. Image courtesy of Wikipedia.

Next, we would kindly ask our readers to take a close look at Table 1 in the Wielgoss paper, which Professor Moran cited in his reply. Taking as an example population Ara-3, the reader will notice that the 10 individuals from that population have 10 different mutations. These mutations are all in a polymorphic state – that is, a single individual (others not sampled may also have the same mutation) possesses a particular mutation, whereas the other individuals in that population do not possess that mutation, but have different ones instead. None of the mutations is therefore fixed, because if it were, all of the sampled individuals would have that particular mutation – for example, 756,799 C-T would be present in all 10 individuals – in addition to their own mutations. Accordingly, every new mutation on its way to fixation has to pass through a polymorphic state. For any given mutation, the probability of fixation is 1/(2N) and the time it takes to achieve fixation is 4N generations.

Lest Professor Moran object that Gillespie’s textbook might be considered hostile to his views, we would now like to quote from another textbook on population genetics. The following quote is taken from Daniel L. Hartl and Andrew G. Clark, Principles of Population Genetics (Fourth Edition, Sinauer Associates, 2007), Chapter 3, Random Genetic Drift, under the heading, “Absorption Time and Time to Fixation”, pages 112-113:

Equations 3.8 and 3.9 are of particular interest when p = 1/(2N), that is, when a new neutral mutation has just occurred and there is one copy in the population. In this case, the probability of eventual fixation is 1/(2N), and, given that the allele is eventually fixed, the average time to fixation is approximately 4N generations. On the other hand, the probability that a new allele is eventually lost is 1 – 1/(2N), and, given that the allele is eventually lost, the average time to loss is approximately 2*ln(2N) generations. In other words, new neutral alleles that are eventually fixed usually take a long time to be fixed, whereas those that are lost are lost very quickly. For the specific example of N = 500, the average new mutation that is eventually fixed requires 2000 generations to be fixed, whereas the average new mutation that is destined to be lost requires fewer than 14 generations to be lost. (Emphases ours – BK & VJT.)

Professor Moran believes that 100 mutations were fixed in each human generation for 5 million years, because that is required in order to explain the differences between human and chimp genomes. Can population genetics supply a model that delivers what is asked of it?

Let us now consider two hypothetical models:

1. In every human generation there was just a single couple that left descendants (effective population size 2Ne = 2), while all others were infertile or killed, so all new 100 mutations that appeared (scattered across some 3,000,000,000 possible sites in the genome) were fixed in the descendants.

2. In all individuals of one generation (2Ne can have any value), all the new mutations were of the same type and happened at the same sites, so regardless of which individuals mated, all descendants acquired the same mutations. This same process continued for thousands of generations, with various mutations.

The first model would require continual inbreeding, and the second, continual miracles. Neither model appears credible to us; nor do we believe Professor Moran would espouse either of these models. It is important to note, however, that that both models have one thing in common, which is why they both work: all of the mutations fix without having to pass through the polymorphic state. We suspect that Professor Moran’s back-of-the-envelope-calculations which he referred to (see the footnote below), share this same feature. We would therefore kindly ask Professor Moran to provide a numerical value for Ne that does the job, for a model that’s capable of delivering what he needs, which is: 100 new mutations being fixed in each human generation over a period of 5,000,000 years.

The pattern of fixation also needs to be explained

In our previous post, we referred to an article by Rasmus Nielsen et al., titled, A Scan for Positively Selected Genes in the Genomes of Humans and Chimpanzees (PLoS Biology, 3(6): e170. doi:10.1371/journal.pbio.0030170, published May 3, 2005), in particular to Figure 1 that shows that multiple mutations (up to 21) have become fixed in thousands of different proteins, leading us to state:

In short: it is the pattern of fixation which neither the theory of neutral evolution nor the neo-Darwinian theory of natural selection, nor any combination of the two, can adequately explain.

Until now, Professor Moran has provided no evidence that would contradict our statement. At this point we would kindly ask him to take a close look at two relevant articles, in order to better understand the challenges that the pattern of fixation poses for population genetic modeling:

Behe MJ, Snoke DW (2004) Simulating evolution by gene duplication of protein features that require multiple amino acid residues. Protein Science 13:10, pp. 2651-2664, doi:10.1110/ps.04802904

and

Lynch M (2005) Simple evolutionary pathways to complex proteins. Protein Science 14:9, pp. 2217-2225, doi:10.1110/ps.041171805.

Behe and Snoke’s response to Lynch can be found here.

Hundreds of orphan genes that characterize each species: why doesn’t Professor Moran recognize their existence?

Karyotype of a human male. (A karyotype is a complete set of the chromosomes of a cell, usually arranged in pairs and in descending order of size.) Image courtesy of the National Human Genome Research Institute and Wikipedia.

We would also like to remind Professor Moran that a major issue from the start of this discussion [on macroevolution] still remains open. In a previous post, titled, So, why are the human and chimpanzee/bonobo genomes so similar? A reply to Professor Larry Moran (March 21, 2014), Torley wrote:

In conclusion, I’d like to point out that Professor Moran nowhere addressed the problem of the origin of orphan genes in his reply, so he didn’t really answer the first argument in my previous post, which was that we cannot claim to understand macroevolution until we ascertain the origin of the hundreds of chemically unique proteins and orphan genes that characterize each species.

Moran then responded:

I didn’t discuss orphan genes because it’s irrelevant to either of the points I was making. It has nothing to do with the question of human/chimp sequence similarity and it has nothing to do with the abundant evidence in support of macroevolution. Besides, I don’t accept his premise that there are hundreds of unique genes that characterize each species.

This is astonishing. Leaving aside the fact that orphan genes obviously do have an impact on sequence similarity and on the view of macroevolution, a prominent biochemist like Moran would normally be expected to give reasons for his refusal to recognize the reality of hundreds of unique genes and proteins found in the sequenced genomes of all species (on this point, see this paper by Kozulic). The reasons for his refusal can only be based on a defect which he has discovered in the experimental data, or in the logic underlying the interpretation of the data, or both. We hope that Professor Moran will use this opportunity to provide us with his reasons.

Is Professor Moran a Darwinist, protestations to the contrary notwithstanding?

On many occasions, Professor Moran has publicly stated that he does not consider himself a Darwinist. We would be in perfect agreement with him, and we ourselves would be happy to be called evolutionists, based on the following simple definition of evolution (Gillespie, p. xi): “Evolution is the change in the frequencies of genotypes through time, perhaps due to their differences in fitness.” But there is one crucial issue that divides us: the fundamental claim of Darwinism that variations among individuals of one species are fundamentally no different in kind from the variations between individuals of different species. We disagree. As long as Professor Moran accepts and promotes the above claim, he remains (in this important respect) a Darwinist, notwithstanding his protestations to the contrary.

To avoid any misunderstandings, we would like to say that we regard population genetics as an exact science. One of us (BK) views the present relationship between Darwinism and population genetics as follows: Darwinism is torturing population genetics to deliver what it cannot deliver – models that do not contradict what we currently know about the differences between species, which have been identified in the sequenced genomes of several thousand species.

Given the vital importance of population genetics models, we hope Professor Moran will answer all of the above questions. Since he is a biochemist, he can hardly be expected to know all the intricacies of population genetics (and neither would we claim to possess such knowledge), so we would encourage him to consult the textbooks and ask for assistance from his colleagues.

Footnote

In his February 28 post, titled, Why are the human and chimpanzee/bonobo genomes so similar?, Professor Moran wrote:

The human and chimp genomes are 98.6% identical or 1.4% different. That difference amounts to 44.8 million base pairs distributed throughout the entire genome. If this difference is due to evolution then it means that 22.4 million mutations have become fixed in each lineage (humans and chimp) since they diverged about five million years ago.

The average generation time of chimps and humans is 27.5 years. Thus, there have been 185,200 generations since they last shared a common ancestor if the time of divergence is accurate. (It’s based on the fossil record.) This corresponds to a substitution rate (fixation) of 121 mutations per generation and that’s very close to the mutation rate as predicted by evolutionary theory.

67 Replies to “Branko Kozulic responds to Professor Moran

  1. 1
    wd400 says:

    Seriously, ID people, are you not embarrassed by this?

  2. 2
    VunderGuy says:

    @wd400

    Ummm…are you going to respond by something other than an emotional smokescreen?

  3. 3
    bornagain77 says:

    wd400 you ask:

    Seriously, ID people, are you not embarrassed by this?

    Not to pick on you, but that is a highly ironic question coming from someone who believes that his brain, which has more switches than all the computers and routers and Internet connections on Earth, came about by totally unguided processes. Moreover, you believe this ‘beyond belief’ complexity happened by accident, in spite of the fact that you can’t even demonstrate the origination of a single protein of that ‘beyond belief’ complexity by Darwinian processes!

    Stephen Meyer Critiques Richard Dawkins’s “Mount Improbable” Illustration – video
    http://www.youtube.com/watch?v=7rgainpMXa8

    References:

    Human brain has more switches than all computers on Earth – November 2010
    Excerpt: They found that the brain’s complexity is beyond anything they’d imagined, almost to the point of being beyond belief, says Stephen Smith, a professor of molecular and cellular physiology and senior author of the paper describing the study: …One synapse, by itself, is more like a microprocessor–with both memory-storage and information-processing elements–than a mere on/off switch. In fact, one synapse may contain on the order of 1,000 molecular-scale switches. A single human brain has more switches than all the computers and routers and Internet connections on Earth.
    http://news.cnet.com/8301-2708.....2-247.html

    I guess, I am embarrassed wd400! I’m embarrassed that a fellow human could actually be so gullible to believe what you believe!

  4. 4
    Upright BiPed says:

    #1

    Well, no.

    But, I freely admit I’ve all but stopped following what Dr Moran has to say. He clearly fled from a conversation 3 years ago regarding the IC system required for Darwinian evolution to exist in the first place. I therefore know how he works.

  5. 5
    NickMatzke_UD says:

    Seriously this post is the worst one I’ve ever read on UD. If you can’t get it through your thick skulls how the neutral mutation rate equals the neutral substitution rate under simple conditions, which is explained in hundreds of textbooks and websites, there is no hope for you scientifically. Heck, you could build a simulation in R to show it in a few minutes.

    Hints: if a population has constant size 10, and each individual had 1 new neutral mutation per generation, how many mutations enter THE POPULATION each generation?

    If each of the 10 critters lays 2 eggs (clones, except for mutations) and then dies, and the eggs hatch but on average only 50% of eggs makes it to adulthood, how many of the first generation’s mutations will typically make it into generation #2? Will some of generation #1’s mutation go up in frequency sometimes?

    Play the scenario forward. Does the size 10 population just keep growing the number of neutral mutations in the population each generation?

  6. 6
    wd400 says:

    This is becoming quite the performance piece. It’s one thing to not know much
    about population genetics, but quite another to presume your hasitly cobbled
    together ideas have found a flaw an entire field…

    To take a few small examples, you say

    But in our view there has never been any dispute on this point. Indeed, in our post (April 5, 2014), we treated the quoted figure from that study of 35 mutations as fixed mutations (see below), in order to show that the fixation rate Professor Moran stated for the human population was over five orders of magnitude greater

    You showed the fixation rate was higher, given the absolute
    number
    of fixations? Have you considered what the rate part means?

    As you’ve been told, the E. coli genome is ~3 orders of magnitude smaller
    than the human genome, and the per-nucleotide mutation rate is ~2 orders of
    magnitude lower. The E coli experiment is consistent with the key idea of the
    neutral theory, that for neutral variant population fixation rate is equal to
    the invdividual mutation rate (for the nucleotide, gene or genome).

    But if ? is 1E10 per bp per generation then 1/? equals 1E10, or 10 billion. Since the effective human population size N was 10,000 or less during most of the Paleolithic era, it would follow that N << 1/?, "leading to a population devoid of variation," as Gillespie states. This runs completely contrary to the scenario Professor Moran is proposing: he maintains that there was sufficient variation to fix 100 mutations in each generation, from five million years ago to the present.)

    The human mutation rate is more on the order of 1E-8.

    One meausure of genetic diversity is “nucleotide diversity” – the probability
    that a randomly selected nucleotide would differ from another individuals (or
    chomorome’s) version at the same position. Basically heterozygosity at the
    nucleotide level. Under neutrality

    nucleotide diversity ~ 4.Ne.u = 4*1E4*1E-8 = 0.0004

    Actual human nucleotide diversity ~0.001, so about what we’d expect given most
    diversity being neutral (population structure and a slightly higher mutation
    rate probably also add to the small difference). We are pretty ‘devoid of
    diversity’ compared to many species, but at abut the level neutral theory
    predicts.

    This bit
    This runs completely contrary to the scenario Professor Moran is proposing:
    he maintains that there was sufficient variation to fix 100 mutations in each
    generation, from five million years ago to the present.)

    is irrelevant. The point Gillespe is making (or seems to be, devoid of context)
    is that the path th fixation takes longer in large mutations, so there is more
    standing diversity. When fixation is quick (smaller pops) the fixation happens
    more rapidly so there are less genes “in transit” at any time and lower standing
    diversity.

    First, since we are talking about nucleotide mutations here, why doesn’t he apply the value for the mutation rate per nucleotide in his calculation?

    Because you were asking about the total number of fixations, not the fixation
    rate per base.

    Our second, related question is: since the dispute between us is not about the fixation rate of individual genomes(?), then why does he use the value for the mutation rate per individual genome?

    Because for neutral variants, the population fixation rate is equal to
    individual mutation rate. That’s the whole point!

    These mutations are all in a polymorphic state

    No. The first column contains different populations, each of the listed
    variatns are fixed within the sampled population.

    For any given mutation, the probability of fixation is 1/(2N)

    Exactly.
    For each neutral mutation P(fixation) = 1/(2N), variants arrive in the
    population at a rate = 2N.u (i.e. the mutation rate per [unit] * the number
    of chromosomes) so the expected fixation rate (s) is

    s = 2N.u * 1/(2N)
    = u

    In our previous post, we referred to an article by Rasmus Nielsen et al., titled, A Scan for Positively Selected Genes in the Genomes of Humans and Chimpanzees (PLoS Biology, 3(6): e170. doi:10.1371/journal.pbio.0030170, published May 3, 2005), in particular to Figure 1 that shows that multiple mutations (up to 21) have become fixed in thousands of different proteins, leading us to state

    As I showed in the last comment, this is precisely what we expect to see.

    You used 1,000 bases a a gene size. So, under neutrality the fixation rate is
    equal to the per individual mutation rate

    s = u
    = 1E-8 per nucleotide * 1e3 nucleotides per gene + 2e5 generations
    = 2 mutations per lineage

    Meaning the expected number of differences per gene is 4 (uman and chimps have
    both been evolving, after all). As i said last time, the average number of
    differences is actually lower than this expectation, thanks to negative
    selection.

    The number of basic errors you have made in these posts is amazing. Don’t you
    think it’s time to either learn some intro to pop. gen. or give up on this
    crusade?

  7. 7
    wd400 says:

    re-posted with blockquotes sorted out:

    This is becoming quite the performance piece. It’s one thing to not know much
    about population genetics, but quite another to presume your hasitly cobbled
    together ideas have found a flaw an entire field…

    To take a few small examples, you say

    But in our view there has never been any dispute on this point. Indeed, in our post (April 5, 2014), we treated the quoted figure from that study of 35 mutations as fixed mutations (see below), in order to show that the fixation rate Professor Moran stated for the human population was over five orders of magnitude greater

    You showed the fixation rate was higher, given the absolute numberof fixations? Have you considered what the rate part means?

    As you’ve been told, the E. coli genome is ~3 orders of magnitude smaller
    than the human genome, and the per-nucleotide mutation rate is ~2 orders of
    magnitude lower. The E coli experiment is consistent with the key idea of the
    neutral theory, that for neutral variant population fixation rate is equal to
    the invdividual mutation rate (for the nucleotide, gene or genome).

    But if ? is 1E10 per bp per generation then 1/? equals 1E10, or 10 billion. Since the effective human population size N was 10,000 or less during most of the Paleolithic era, it would follow that N 1/?, “leading to a population devoid of variation,” as Gillespie states. This runs completely contrary to the scenario Professor Moran is proposing: he maintains that there was sufficient variation to fix 100 mutations in each generation, from five million years ago to the present.)

    The human mutation rate is more on the order of 1E-8.

    One meausure of genetic diversity is “nucleotide diversity” – the probability
    that a randomly selected nucleotide would differ from another individuals (or
    chomorome’s) version at the same position. Basically heterozygosity at the
    nucleotide level. Under neutrality

    nucleotide diversity ~ 4.Ne.u = 4*1E4*1E-8 = 0.0004

    Actual human nucleotide diversity ~0.001, so about what we’d expect given most
    diversity being neutral (population structure and a slightly higher mutation
    rate probably also add to the small difference). We are pretty ‘devoid of
    diversity’ compared to many species, but at abut the level neutral theory
    predicts.

    This bit
    This runs completely contrary to the scenario Professor Moran is proposing:
    he maintains that there was sufficient variation to fix 100 mutations in each
    generation, from five million years ago to the present.)

    is irrelevant. The point Gillespe is making (or seems to be, devoid of context)
    is that the path th fixation takes longer in large mutations, so there is more
    standing diversity. When fixation is quick (smaller pops) the fixation happens
    more rapidly so there are less genes “in transit” at any time and lower standing
    diversity.

    First, since we are talking about nucleotide mutations here, why doesn’t he apply the value for the mutation rate per nucleotide in his calculation?

    Because you were asking about the total number of fixations, not the fixation
    rate per base.

    Our second, related question is: since the dispute between us is not about the fixation rate of individual genomes(?), then why does he use the value for the mutation rate per individual genome?

    Because for neutral variants, the population fixation rate is equal to
    individual mutation rate. That’s the whole point!

    These mutations are all in a polymorphic state

    No. The first column contains different populations, each of the listed
    variatns are fixed within the sampled population.

    For any given mutation, the probability of fixation is 1/(2N)

    Exactly.
    For each neutral mutation P(fixation) = 1/(2N), variants arrive in the
    population at a rate = 2N.u (i.e. the mutation rate per [unit] * the number
    of chromosomes) so the expected fixation rate (s) is

    s = 2N.u * 1/(2N)
    = u

    In our previous post, we referred to an article by Rasmus Nielsen et al., titled, A Scan for Positively Selected Genes in the Genomes of Humans and Chimpanzees (PLoS Biology, 3(6): e170. doi:10.1371/journal.pbio.0030170, published May 3, 2005), in particular to Figure 1 that shows that multiple mutations (up to 21) have become fixed in thousands of different proteins, leading us to state

    As I showed in the last comment, this is precisely what we expect to see.

    You used 1,000 bases a a gene size. So, under neutrality the fixation rate is
    equal to the per individual mutation rate

    s = u
    = 1E-8 per nucleotide * 1e3 nucleotides per gene + 2e5 generations
    = 2 mutations per lineage

    Meaning the expected number of differences per gene is 4 (uman and chimps have
    both been evolving, after all). As i said last time, the average number of
    differences is actually lower than this expectation, thanks to negative selection.

    The number of basic errors you have made in these posts is amazing. Don’t you
    think it’s time to either learn some intro to pop. gen. or give up on this
    crusade?

  8. 8
    humbled says:

    We’ll give up on this crusade when you folks admit your position is based on faith and wishful thinking and stop teaching this rubbish to our kids.

  9. 9
    vjtorley says:

    Hi Nick and wd400,

    Thank you both for your comments. May I remind you that Branko Kozulic, the co-author of this post, is a biochemist who has published about 30 scientific papers and who is the inventor or co-inventor of numerous Patents (18 of which are issued in the USA). He is also well-read in the field of population genetics. Dr. Kozulic is a very busy man, but if he wishes to pass on any responses to me, I shall keep you posted.

    wd400: You critiqued our figure for the human mutation rate. But in our post, we quoted Professor Moran, who wrote: “As for the question, I can’t really answer it because I don’t know what John Gillespie means by the mutation rate (μ). If it’s 10-10 per bp per generation then 1/μ equals 1010, or 10 billion.” In criticizing us, you are also criticizing Professor Moran.

    I have checked with BioNumbers at http://bionumbers.hms.harvard......#038;ver=9 and they say that 2.5×10-8 is a reasonable estimate of the average mutation rate per nucleotide site per generation, quoting Nachman MW, Crowell SL. Estimate of the mutation rate per nucleotide in humans. Genetics. 2000 Sep, 156(1):297-304. They then add: “There is a 3 order of magnitude difference between mutation/bp/replication and mutation/bp/sexual generation as that is the number of cell divisions prior to sperm formation (there are ~400 cell divisions in a male of age 30 (Drost and Lee 1995 Vogel and Motulsky 1997)).”

    To be fair to Professor Moran, he did give the correct figure of 1.0×10-10 mutations per bp per replication in another post: http://sandwalk.blogspot.jp/20.....irect.html . He may have simply expressed himself carelessly in the other post he wrote (after all, he is a busy man).

    In any case, the point we made in our post regarding the relative magnitudes of N (the population size) and the mutation rate (μ) [mu] remains valid. As Gillespie put it: “If 1/μ << N, the time scale of mutation is much less than drift, leading to a population with many unique alleles. If N << 1/μ, the time scale of drift is shorter, leading to a population devoid of variation." Since N is about 10,000 for most of the Paleolithic, it won't make much difference whether μ is 10-10 or 2.5×10-8.

    You also wrote: “As you’ve been told, the E. coli genome is ~3 orders of magnitude smaller than the human genome, and the per-nucleotide mutation rate is ~2 orders of magnitude lower.”

    Thanks, but we already knew that. I said as much in this comment at http://www.uncommondescent.com.....ent-495392 , dated April 6, where I wrote:

    Thank you for your post. I had anticipated your criticism:

    The E. coli genome is more than 600 times smaller than the human genome and has a mutation rate ~ 2 orders of magnitude lower (in part because there are multiple cell divisions per generation in animals).

    I was waiting for Professor Moran to come out and say something like that. To my surprise, he didn’t.

    You also wrote: “The point Gillespe is making (or seems to be, devoid of context) is that the path to fixation takes longer in large mutations, so there is more standing diversity.”

    So you admit that you haven’t read Gillespie (chapter 2 of his book is available online). As for your comment that “the path to fixation takes longer in large mutations”, don’t you mean large populations? Once again, you’re not telling us anything new: in our post, we explicitly state that “the time it takes to achieve fixation is 4N generations.”

    Finally, you appear to have missed the point of our quotation of the article by Rasmus Nielsen et al., titled, A Scan for Positively Selected Genes in the Genomes of Humans and Chimpanzees (PLoS Biology, 3(6): e170. doi:10.1371/journal.pbio.0030170 at http://www.plosbiology.org/art.....io.0030170. The point we were making was that “multiple mutations (up to 21) have become fixed in thousands of different proteins.” We referred Professor Moran to Figure 1. That’s what we wanted Professor Moran to explain. We’re still waiting.

  10. 10
    ppolish says:

    Nick, thanks for the suggestion to check out the “hundreds of textbooks”. But I think I will wait until they are re-written in the relatively near future:) Its a time management / procrastination thing…

  11. 11
    wd400 says:

    He is also well-read in the field of population genetics

    He would fail the pop. gen. section of intro to genetics.

    I really am amazed that you can’t see the errors in this, I only hope your fellow travellers can convince you of them, because I don’t know how I could spell them out more clearly than I already have.

  12. 12
    TruthCrusader says:

    Torley, your intentions are noble, but I suggest you walk away from this issue and pretend it never happened.

    The evidence for evolution on the whole is limited, but population genetics and neutral drift have been established experimentally and mathematically. You, or whoever is advising you has made some basic errors in the above.

  13. 13
    Joe says:

    Umm knowing population genetics is one thing. Applying population genetics to the real world is quite another.

    What population has a constant population size of 10? For that matter what population is ever constant in size?

    Population genetics, great on paper for those who can ignore reality.

  14. 14
    Joe says:

    If understanding reality means I would fail at population genetics, I will gladly fail at population genetics. However I could easily play the game of population genetics and score as high as anyone.

  15. 15
    NickMatzke_UD says:

    10
    ppolishApril 10, 2014 at 4:09 pm
    Nick, thanks for the suggestion to check out the “hundreds of textbooks”. But I think I will wait until they are re-written in the relatively near future:) Its a time management / procrastination thing…

    ID = anti-intellectualism = being dumb by choice

  16. 16
    NickMatzke_UD says:

    Umm knowing population genetics is one thing. Applying population genetics to the real world is quite another.

    What population has a constant population size of 10? For that matter what population is ever constant in size?

    Population genetics, great on paper for those who can ignore reality.

    If you actually bothered to get off your lazy butt and think about it for half a second, you would realize that population size cancels out of the process. More individuals = slower fixation time per locus, but also more individuals = more new mutations into the population per generation.

    The logic about how a small percentage of neutral mutations eventually randomly fix in the population (fixing=substitution) is exactly the same whether you have 10 individuals or 10000000. I started with 10 only because it is amazingly clear that you guys aren’t getting the absolutely introductory basics of this topic.

  17. 17
    Mung says:

    NickMatzke_UD:

    Seriously this post is the worst one I’ve ever read on UD. If you can’t get it through your thick skulls how the neutral mutation rate equals the neutral substitution rate under simple conditions, which is explained in hundreds of textbooks and websites, there is no hope for you scientifically. Heck, you could build a simulation in R to show it in a few minutes.

    I’ve been wanting to explore R. Post the code or a link to it? I suggest a gist on GitHub.

  18. 18
    Mung says:

    Nick:

    Seriously this post is the worst one I’ve ever read on UD.

    No way! You’ve been lurking here a long time, surely one of my posts would qualify as the worst ever. I work hard at it. and now my self-image has been shattered. Nick, how could you?

  19. 19
    Barry Arrington says:

    Dr. Matzke @ 15. Seriously? I would have supposed that a “neener, neener, neener; you’re a bunch of poopyheads” response would have been beneath the dignity of a Ph.D. holding scientist such as yourself. I stand corrected.

  20. 20
    ppolish says:

    Nick, ppolish does not = ID. That is your first mistake. Also, it is “dumb by design” not “dumb by choice”. Strike two.

    What a great time to be a Physics student
    btw. LHC/CMB giving great new insights. Crappy time to be an EvoBio student, however, learning dogma soon to be outdated

  21. 21
    NickMatzke_UD says:

    So you admit that you haven’t read Gillespie (chapter 2 of his book is available online). As for your comment that “the path to fixation takes longer in large mutations”, don’t you mean large populations? Once again, you’re not telling us anything new: in our post, we explicitly state that “the time it takes to achieve fixation is 4N generations.”

    Yes, wd400 meant to say populations there.

    Finally, you appear to have missed the point of our quotation of the article by Rasmus Nielsen et al., titled, A Scan for Positively Selected Genes in the Genomes of Humans and Chimpanzees (PLoS Biology, 3(6): e170. doi:10.1371/journal.pbio.0030170 at http://www.plosbiology.org/art…..io.0030170. The point we were making was that “multiple mutations (up to 21) have become fixed in thousands of different proteins.” We referred Professor Moran to Figure 1. That’s what we wanted Professor Moran to explain. We’re still waiting.

    No, your main argument with reality was about this:

    The crux of our dispute with Professor Moran, as agreed by both sides (see above) is the feasibility of 22 million neutral mutations being fixed in the human population, over a period of five million years. These mutations are nucleotide mutations.

    The 22 million neutral substitutions are easy to account for once you get why the neutral mutation rate and substitution rate are equal.

    Re: Rasmus’s study, this is about SELECTION in GENES, not NEUTRAL PROCESSES across the GENOME. Only ~1% of the genome is genes. So it’s not particularly relevant to assessing the overall amount of substitution across the genome.

    You’ve never even stated what the problem is, exactly, raised by Rasmus’s study, you are just pointing and shouting like someone who just saw a zebra for the first time. Amongst the things someone interested in not embarrassing themselves (you are far past this, I’m afraid) would think about:

    – Genes have many different sizes. Some are 30 times longer than others. Bigger genes will on average have more substitutions than smaller genes.

    – In a stochastic process, even two genes of the same length can accumulate different numbers of mutations, just by chance

    – Genes are under much stronger selection than most of the rest of the genome. This can reduce substitution rates (purifying selection) or increase them (directional selection) relative to the background neutral rate. Thus, variation in the number of substitutions between genes is not surprising. Neutral theory is not in control, when there is selection.

    In other words: duh!! Why are you inflicting this stuff on the internet!?! Why is this Kozulic guy on the board of BIO-Complexity (IIRC) if he can’t even get these absolute simple basic considerations right??

  22. 22
    Mung says:

    NickMatzke_UD:

    Hints: if a population has constant size 10, and each individual had 1 new neutral mutation per generation, how many mutations enter THE POPULATION each generation?

    Well, in that model, I’d be wondering just how many mutations LEAVE the population each generation.

    And since my skull is ESPECIALLY thick, I’d figure as follows:

    10 new individuals are poofed into existence, each with a new mutation. They replace 10 individuals, who are immediately poofed out of existence who had themselves each had one new mutation, but that mutation is now lost, because the rules say we have to maintain a constant population size.

    I just don’t see how any mutation would become fixed.

    But then, I’ll be the first to admit I’m no population geneticist.

    worst post ever? please?

  23. 23
    NickMatzke_UD says:

    22
    MungApril 10, 2014 at 6:31 pm
    NickMatzke_UD:

    Hints: if a population has constant size 10, and each individual had 1 new neutral mutation per generation, how many mutations enter THE POPULATION each generation?

    Well, in that model, I’d be wondering just how many mutations LEAVE the population each generation.

    That it why I wrote this in my hints: If each of the 10 critters lays 2 eggs (clones, except for mutations) and then dies, and the eggs hatch but on average only 50% of eggs makes it to adulthood, how many of the first generation’s mutations will typically make it into generation #2?

    And since my skull is ESPECIALLY thick, I’d figure as follows:

    10 new individuals are poofed into existence, each with a new mutation. They replace 10 individuals, who are immediately poofed out of existence who had themselves each had one new mutation, but that mutation is now lost, because the rules say we have to maintain a constant population size.

    I just don’t see how any mutation would become fixed.

    But then, I’ll be the first to admit I’m no population geneticist.

    worst post ever? please?

    It’s a strong contender. You are leaving out the fact that mutations are inherited. Again: duh!

  24. 24
    lpadron says:

    Barry,
    Such behavior IS beneath a PhD, but not beneath that of an attention seeking a-hole. Fortunately, Matzke is one of those as well.

  25. 25
    Mung says:

    Nick:

    It’s a strong contender. You are leaving out the fact that mutations are inherited. Again: duh!

    Not in my model! Duh!

    I know Nick, I’m just jerking your chain, wondering how far your stereotyping is willing to take you, and vying for the “worst ever” status, as always. 🙂

    Are you saying the same population genetics models apply regardless of whether we are discussing bacteria or humans?

    Actually you don’t have to answer that if you don’t want to. I had intended to ask if we weren’t comparing “apples to oranges” independently of anything you had written.

    But since you seem to explicitly raise the two different scenarios and since you do seem to imply the same math/models apply to both, if you would be so kind.

    Thank you.

    p.s. I would love to see that R code.

  26. 26
    Mung says:

    As with all models, you should consider the importance of factors we ignore.

    – Population Biology: Concepts and Models

  27. 27
    Mung says:

    ..the density-independent model cannot explain most populations we see in nature.

    – Population Biology: Concepts and Models

  28. 28
    Mung says:

    We first examine the simplest model of population growth of a single species. The model begins with two assumptions of density independence:

    * The rate of births is proportional to the number of individuals present.

    * The rate of deaths is proportional to the number of individuals present.

    – Population Biology: Concepts and Models

    Help me out here Nick. Assume I’m just an ignorant rube taken in by the slick publications of the Discovery Institute. Pretend that my soul and the very soul of science is at stake and that you care deeply about both.

    What are the assumptions of a constant population size model? In what way do they differ from the assumptions of a density independence model?

  29. 29
    NickMatzke_UD says:

    25 Mung
    April 10, 2014 at 8:22 pm

    Nick:

    It’s a strong contender. You are leaving out the fact that mutations are inherited. Again: duh!

    Not in my model! Duh!

    I know Nick, I’m just jerking your chain, wondering how far your stereotyping is willing to take you, and vying for the “worst ever” status, as always. 🙂

    Well, what you said was approximately as silly as the dreck in the opening post, so good job, I guess.

    Are you saying the same population genetics models apply regardless of whether we are discussing bacteria or humans?

    Actually you don’t have to answer that if you don’t want to. I had intended to ask if we weren’t comparing “apples to oranges” independently of anything you had written.

    But since you seem to explicitly raise the two different scenarios and since you do seem to imply the same math/models apply to both, if you would be so kind.

    The popgen models, for the simplest cases we are discussing here, are very similar. The differences are e.g. haploid vs. diploid populations, or n vs. 2n numbers of individual spots at a particular locus. The biggest difference is that a truly clonal population with no sex will not have recombination, in effect each genome is one big locus. But this doesn’t change the average rate of substitution. For the purposes of thinking about the fate of 1 mutation it doesn’t matter much.

    The model we are discussing and that VJ Torley and Kozulic can’t seem to grasp is basically just a stochastic sampling model. The chance of any particular mutation eventually fixing is equal to its frequency in the population. For a new mutation, the starting frequency is 1/2N in a diploid population. It’s the same logic as winning the lottery. Most people don’t win, but wins happen nevertheless. The probability is equal to the # winning tickets / # of total tickets.

    So, Mung: what do you think of vjtorley/Kozulic’s argument? Don’t just snipe from the sidelines, exercise your brain a little.

    Thank you.

    p.s. I would love to see that R code.

    I posted it awhile ago, I don’t know why it’s not showing up.

  30. 30
    NickMatzke_UD says:

    28
    MungApril 10, 2014 at 8:51 pm
    We first examine the simplest model of population growth of a single species. The model begins with two assumptions of density independence:

    * The rate of births is proportional to the number of individuals present.

    * The rate of deaths is proportional to the number of individuals present.

    – Population Biology: Concepts and Models

    Help me out here Nick. Assume I’m just an ignorant rube taken in by the slick publications of the Discovery Institute. Pretend that my soul and the very soul of science is at stake and that you care deeply about both.

    What are the assumptions of a constant population size model? In what way do they differ from the assumptions of a density independence model?

    Well, for starters, you are confusing population biology and population genetics. These are different things…

    What are the assumptions of a constant population size model? In what way do they differ from the assumptions of a density independence model?

    These are models of how populations of critters grow on ecological timescales, i.e. over a few years. The population genetics models operate on evolutionary timescales, thousands or millions of years, where the short-term ecological processes are mostly noise that averages out. There are detailed qualifications that could be made for every statement there, but that’s the big picture.

    Can you see, even a little, how dealing with misunderstandings of this sort of catastrophic magnitude, i.e., confusing entire fields, might be vexing to a biologist? Particularly on a forum where the people with these same sorts of misunderstandings also declare the biologists’ field to be bunk and evil to boot?

  31. 31
    Andre says:

    NickMatzke_UD

    Lets have some fun shall we?

    Neutral Theory and random genetic drift produce genomes that differ by 22 million positions if we take the fossil evidence at face value and assume that chimps and humans last shared a common ancestor about 5 million years ago

    Larry Moran

    So we have a thumb suck and an assumption to work with here not any facts, so you are basing your answers on what you believe but not on what you know. Religious allot Nick?

    Seriously this post is the worst one I’ve ever read on UD. If you can’t get it through your thick skulls how the neutral mutation rate equals the neutral substitution rate under simple conditions, which is explained in hundreds of textbooks and websites, there is no hope for you scientifically. Heck, you could build a simulation in R to show it in a few minutes.

    Nick Matzke

    Are you saying that we should believe computer generated models? Well let me remind you Global warming is a prime example of computer models being a spectacular flop, have you noticed that “Global warming” has now become “climate change”. Have you ever considered that you can design these programs to do and show exactly the results you believe in? I guess not because your belief is that you are right and everybody else is wrong!

    ID = anti-intellectualism = being dumb by choice

    Nick Matzke

    Nick, firstly I will have to assume that you used the scientific method to measure us as being dumb by choice (you are the distinguished science guy ain’t ya?), otherwise that could just be your opinion and as you very well know, opinions are like a-holes, everybody’s got one! Now Nick it does not take a PHD to understand that you are driven by religion whatever yours may be. The entire premise about science is to gain knowledge, there is no such thing as a stupid question.

  32. 32
    Andre says:

    Nicke Matzke

    One last request, When can we get your book that make Macroevoltion a undeniable fact? Looks like that promise has gone a bit cold!

  33. 33
    Andre says:

    Nick Matzke

    I however would like to explore the following?

    Let us discuss the very, very conservative 1.8% difference in the genome between humans/chimps what happens when this difference turns out to be 25%? What happens then Nick?

    Why are you ignoring ORFANS? Where do they come from Nick?

  34. 34
    Andre says:

    Nick Matzke

    Here is a paper that says the genomes differ by 4%

    http://genome.cshlp.org/content/15/12/1746.long

    And even more

    http://www.answersingenesis.or.....chromosome

    As much as you would object to the paper above as being creationist and thus not peer reviewed I completely understand that these papers are never published in those journals because of your history to censor anything you disagree with. We have on record numerous occasions of you successfully blocking these papers with threats made to publishers.

    I have to try and understand why you are trying so hard to protect your belief system Nick?

  35. 35
    Dr JDD says:

    Please can a cell biologist ask a dumb question? I will readily admit to not being a geneticist and not fully understanding population genetics or particular aspects of these mutational studies (despite having a fairly adequate grasp on molecular biology), but that is how science generally works – you become quite specialist in your area and rely on other people’s expertise. I also say this to remind everyone how dogma gets generated!!

    Anyway, my question is around the estimation of 10e-8 being the mutation rate. If you read this paper here:

    http://www.genetics.org/content/156/1/297.full

    Which I skimmed briefly a few days ago when these discussions came up (trying to understand where the 10e-8 neutral mutation rate came from), the way I see it (I will admit that I have a limited understanding of this) is that it was determined by comparing “pseudogenes” (I have to use quotations as this was 14 yrs ago and I am sure what was a pseudogene then is not necessarily still) from humans and chimps over several genes and then estimating the mutation rate per base, based on the time since divergence (5mya), an ancestral population size of 10e4, and a generation time of 20y.

    These parameters sound a lot like the parameters discussed here. I realise I have not given this much thought and delved into it (population genetics was one of my least favourite topics I will admit), but it almost seems to me as though a mutation rate, that was determined with x, y and z factors, is being plugged back into a reverse calculation with the same x, y and z factors and getting the expected result of the number of neutral mutations. To put it differently (how I am seeing it, which I will readily admit is probably wrong), the mutation rate being used was determined essential by comparing chimps and human divergence in the first place, then it was calculated based on the differences between the two but now is being used to justify the differences between the two in the same time frame used in both calculations (and same ancestral population/generation time) and as evidence for the neutral theory being correct and fitting with humans evolving from chimps? I must be completely missing how the mutation rate was determined??

    However secondly, if this rate was determined from apparent “pseudogenes”, why are we only saying it accounts for the 22.4m differences between the chimps and humans, which I believe is the estimated difference based on actual coding genes? Or does this difference account as well for pseudogenes? It certainly cannot account for all the “non-coding” genetic material as there would certainly be more than 22.4m differences then.

    Apologies for the potentially dumb question(s).

    JD

  36. 36
    Joe says:

    Matzke:

    If you actually bothered to get off your lazy butt and think about it for half a second, you would realize that population size cancels out of the process.

    That’s what you say, Nicky.

    More individuals = slower fixation time per locus, but also more individuals = more new mutations into the population per generation.

    Yes I know, Nicky. You still cannot demonstrate fixation of neutral mutations in a natural population.

    Thew only way to get a neutral mutation fixed is either by severe bottleneck or design.

    The logic about how a small percentage of neutral mutations eventually randomly fix in the population (fixing=substitution) is exactly the same whether you have 10 individuals or 10000000.

    There isn’t any logic behind population genetics nor neutral theory.

    I started with 10 only because it is amazingly clear that you guys aren’t getting the absolutely introductory basics of this topic.

    LoL! The basics are OK but do not translate over to the real world. That is what you need to do- how us how pop genetics translates over to the real world. Unfortunately for you, you can’t.

  37. 37
    Joe says:

    22 million neutral mutations are easy to account for by post hoc and ad hoc untestable explanations.

    That is most likely how Kimura did it- post hoc/ ad hoc rationalizations.

  38. 38
    TSErik says:

    Matzke embodies Alinsky in demonizing, and attempting to shame through assertion because his position cannot stand on it’s own.

    I’m curious, why is Matzke so threatened by ID?

  39. 39
    scordova says:

    Dr. Torley,

    I’m sorry I must sympathize with Nick Matzke (puke) and WD400 objections, but I feel some obligation to ask you to at least pause and reconsider.

    The YEC Creationist genetics model, Mendel’s Account agrees to great degree with Larry Moran, Nick Matzke, and WD400. Mendel’s accountant was developed by John Sanford (applied geneticist), Walter ReMine (ID author), John Baumgardner (Princeton and Sandia Lab Scientist), Wes Brewer (MIT PhD), Paul Gipson (Professor of Population Genetics), Robert Carter (PhD genetic engineer and population geneticist), several un-named guilty parties. Mendel’s accountant was featured at the Cornell conference.

    I wrote about it here last year:
    If not Rupe and Sanford, would you rather believe Wiki

    The problem is not fixation, the problem are things like Muller’s ratchet, Haldane’s ratchet, and the Poisson distribution, Kondrashov’s question, mutational meltdown, and one more thing I’ve yet to write about, “S-coefficient ambiguity”, the twisted meaning of fitness, etc. Here was one criticism of neutral evolution:

    http://www.uncommondescent.com.....king-rate/

    I hate being on the opposite side of the majority ID view, but like the arguments over the 2nd law, I have a responsibility to ID students matriculating through secular universities in science curricula to speak up if I think the ID side should reconsider what they are saying. I could of course be wrong too, but I hope you’ll recognize, not every ID proponent would be enthused to disagree with Dr. Moran on the neutral fixation issue. Neutral evolution has it’s flaws, but this isn’t necessarily one worth going after.

  40. 40
    Upright BiPed says:

    The nice thing about UD is that we have mathematician, physicist, molecular engineer, information theorist, geneticist, student ombudsman Sal here to settle these things for us. It is a great benefit to have someone to decide what questions are worth asking. Soon, Dr Torley will be back to thank Sal for his post.

  41. 41
    scordova says:

    The nice thing about UD is that we have mathematician, physicist, molecular engineer, information theorist, geneticist,

    I’m none of those things, but you show such sarcastic hostility for me disagreeing. Do you have something substantive to say to refute the fact that the ID friendly Cornell papers have some support of the neutral fixation rates?

    Do I always have to be the one to speak up and be the fall guy to criticize our own side when they say something that other IDists privately disagree with? In this case Mendel’s accountant is more in agreement with Dr. Moran, and that is a publicly available pop gen program prominently featured at the Cornell conference.

    There’s too much attempt to save face in these circles, not enough concern for what students are actually learning in ID literature and possibly public blogs. Most of the literature is very accurate, most of what is posted on blogs is pretty good, but we’re not always right.

    I have a duty to speak up, but you took it as an opportunity to take a swipe at me.

  42. 42
    scordova says:

    The nice thing about UD is that we have mathematician, physicist, molecular engineer, information theorist, geneticist,

    That’s extremely insulting. I’m none of those things. You can’t accuse me of deciding what questions can’t be asked.

    FWIW, even though it is humiliating, I’m willing to publicly admit errors. Frankly, I couldn’t live with myself knowing I might be leading people astray:

    Admitting Significant Errors in My Understanding of Physics.

    If I believe something is true I say it. When I’m convinced I have said something that will lead people astray, I make a retraction. I speak my conscience. Simple as that.

  43. 43
    Upright BiPed says:

    It’s your methods Sal. Never cared for them.

    And spare me the speech.

  44. 44
    Upright BiPed says:

    If I believe something is true I say it.

    Oh, you do more than just say it.

  45. 45
    scordova says:

    It’s your methods Sal. Never cared for them.

    And spare me the speech.

    This thread isn’t about me, it’s about fixation rates, you took it as an opportunity to make it awfully personal. The core of what I said is this:

    Mendel’s Accountant agrees to great degree with Larry Moran, Nick Matzke, and WD400.

    You and any one else are free to contest the claim on evidential and theoretical grounds.

    I pleaded with Dr. Torley before to reconsider, and maybe I wasn’t doing a good job, maybe I failed to communicate my belief that lots of IDists accept Kimuras formula, minus some problems as has been laid out in other posts at UD.

    Maybe I wasn’t forthright enough at the time. I’m sorry I didn’t mention Mendel’s accountant enough, but in that post of August 2013, which I believed Dr. Torley read, I thought it was quite evident the Mendel team was is large agreement with Kimura’s forumula, which is the focus of this discussion.

    And spare me the speech.

    Then spare me the insults which have nothing to do with the topic at hand.

  46. 46
    wd400 says:

    JDD,

    The mutatin rate can be determined by directly sequencing relatives, or by scaling up from the cellular mutation rate. The fact phylogenetic, biochemical and directly observed mutation rates are so similar is strong support for most genetic variation being selectively neutral.

    t certainly cannot account for all the “non-coding” genetic material as there would certainly be more than 22.4m differences then.

    Don’t be so certain.There are ~twice as many differences, since both chimps and humans have been evolving their own differences. But otherwise the number is about right (or even a slight over estimate) for SNPs which are the only type of variant we are talking about here.

  47. 47
    Upright BiPed says:

    😐

  48. 48
    niwrad says:

    scordova

    Mendel’s Accountant, as any simulation software, is based on theoretical presuppositions and equations, in this case those of evolutionary population genetics. If these presuppositions/equations are flawed, biased or ad-hoc then Mendel’s Accountant may fail.

    I just wrote what I think of the “equations of evolution” here:

    http://www.uncommondescent.com.....evolution/

    Here it seems to me our vjtorley and Kozulic are doing a great job indeed in criticizing some presuppositions of a sub-theory of evolutionist population genetics.

  49. 49
    wd400 says:

    Andre,

    Here is a paper that says the genomes differ by 4%

    If you take indels into account, which these caclulations don’t. And, of course, since indels can be longer than a single base it takes relatively fewer mutations to achieve the extra few percent difference.

  50. 50
    Dr JDD says:

    Thanks for the explanation wd400. I still think that paper cited though has determined the base mutation rate purely on comparing chimps with humans, and calculated it by using time since divergence, population size estimate, and generation time. I am not questioning neutral rate of evolution (do not have enough knowledge on the subject to do so) – I am questioning the use of 10e-8 rate based on a rate determined with the assumption of chimp to human evolution. And again, I am not saying it is wrong – just asking a question, as it my way of everything in life! But thanks for the response.

    I know we are only talking about SNPs here that’s all fair. I just wonder if they are the only variant that matter, given recent findings within the genetic code.

    Scordova – I admire your clear desire for truth and real science so support what you say and agree with the implications. I too am happy to admit when I am wrong and wish more people would give on each side, admit that there are some good arguments that have validity and don’t just disagree because someone has a different belief system than you and you fear agreeing with any point will validate their system! It doesn’t – seeking truth validates your own beliefs, and those open to truth will see that.

    Thanks,
    JD

  51. 51
    scordova says:

    If these presuppositions/equations are flawed, biased or ad-hoc then Mendel’s Accountant may fail.

    Everyone could be wrong! To assert a trait is neutral one must know the selection coefficient (the S-coefficient). No one knows that, it could be positive one day, and negative another. This is especially true for weakly selected traits.

    The reason the Mendel team was friendly to high rate of neutral mutations getting fixed into a population was they were attempting to show large numbers of bad traits get fixed into a population even if they were deleterious (but only slightly deleterious such that they look neutral).

    Given most mutations might truly be bad, then it’s not outrageous to conservatively say 10% of Moran’s 22,000,000 mutations are harmful to function, thus 2,200,000 harmful mutations would have been fixed into the human population since Chimp/Human divergence. If this is the case, as Kondroshov observed, “Then why aren’t we dead 100 times over?”! 😯

    I’ve suggested the reason we aren’t dead is the maybe we didn’t evolve. A less spectacular explanation is the S-coefficients are automatically re-normalized to make the best of sick offspring the most “fit”.

    The cartoon I provided in my post on fixation shows how the next generation is re-normalized to the best of the sick kids. I showed how deterioration can happen while simultaneously agreeing with the idea of “survival of the fittest” (aka “survival of the sickest”).

  52. 52
    wd400 says:

    I am questioning the use of 10e-8 rate based on a rate determined with the assumption of chimp to human evolution

    And I’m saying you get similar rates if you just sequence families and count up mutations, so the result doesn’t rely on those assumptions (and indeed the fact the results are similar supports those assumptions).

    BTW, you mean 1E-8, the ten is in the “E”

  53. 53
    Dr JDD says:

    And I’m saying you get similar rates if you just sequence families and count up mutations, so the result doesn’t rely on those assumptions (and indeed the fact the results are similar supports those assumptions).

    OK thanks – I did not realise they had sequenced families and found the same rate, that’s interesting. Can you point me towards some of that published work please? Thanks.

    BTW, you mean 1E-8, the ten is in the “E”

    Yes that was a little dumb of me – I have not had to write exponetials in any other form except using superscript for a very long time hence the mistake!#

    JD

  54. 54
    scordova says:

    Slight correction before the Darwinists pounce on me:

    Given most mutations might truly be bad, then it’s not outrageous to conservatively say 10% of Moran’s 22,000,000 mutations are harmful to function, thus 2,200,000 harmful mutations would have been fixed into the human population since Chimp/Human divergence.

    That’s true if the mutations are very nearly neutral, closer than the “neutral box” allows. If we allow that these slightly neutrals are up to the limits of :

    S less than 1/4ne

    then the fixation rate of such deleterious mutations is 50% of the general mutation rate so in that case the fixation rate of slightly deleterious is “only” 1,100,000 harmful mutations. So I guess by that standard we should only be dead 50 times over.

  55. 55
  56. 56
    scordova says:

    Perhaps one of the great ironies regarding Nick, is the very papers he worked so hard to suppress (the Cornell papers), the very papers that got him the label, “Nick Matzke book burner”, are the very ones supporting his position in this thread. Well done, Nick.

  57. 57
    shader says:

    Here’s a tip:

    If you think chimpanzees evolved into homo sapiens, you are not a rational individual.

    HTH

  58. 58
    vjtorley says:

    Sal,

    I would like to thank you for your posts. My latest post is up now:

    http://www.uncommondescent.com.....-im-wrong/

    Thank you again for your advice. I would also like to thank Nick Matzke for his patient efforts to teach us all some population genetics. Cheers, Nick.

  59. 59
    Joe says:

    shader, It ain’t that chimps evolved into homo sapiens. The claim is chimps and homo sapiens share a common ancestor, whatever the heck that was. But your point is still the same.

  60. 60
    Mung says:

    Salvador:

    Do I always have to be the one to speak up and be the fall guy to criticize our own side when they say something that other IDists privately disagree with?

    Is that why you delete my posts from your threads?

    Are you the only one qualified to be a critic?

    You can dish it out but you can’t take it?

  61. 61
    Mung says:

    Salvador:

    The reason the Mendel team was friendly to high rate of neutral mutations getting fixed into a population was they were attempting to show large numbers of bad traits get fixed into a population even if they were deleterious (but only slightly deleterious such that they look neutral).

    Or it could have been a design decision that had more to do with not trying to abstract or code something seen as irrelevant to the purpose of the program.

    Is the source code available somewhere? I’d love to see how it deals with neutral and nearly neutral mutations.

  62. 62
    Mung says:

    Salvador:

    Perhaps one of the great ironies regarding Nick, is the very papers he worked so hard to suppress (the Cornell papers), the very papers that got him the label, “Nick Matzke book burner”, are the very ones supporting his position in this thread. Well done, Nick.

    I hardly even know where to begin, but begin I must.

    No, Salvador, “the Cornell papers” do not support Nick.

    Neutral Mutation does not even appear in the index, nor does Neutral Theory, nor even does Kimura appear in the index.

    There is no entry for Mutation as such. There are three that begin with mutation, such as “mutation accumulation experiments” (references a single page).

    Perhaps the index just sucks.

    I did find references to Kimura on p. 233 and 234, along with references to “the rate of mutation fixation” and “nearly-neutral mutations” on those same pages.

    This is text from that chapter (Can Purifying Natural Selection Preserve Biological Information?):

    The goal of this paper is to explore the biological circumstances (to which Muller alluded) that can make a large fraction of deleterious mutations immune to selection.

    From a previous chapter (Multiple Overlapping Codes):

    In our analysis we have for simplicity assumed that if a mutation has a single beneficial effect and a single deleterious effect, it is counted as neutral. However, that is not realistic… (p. 156)

    Salvador:

    …the Cornell papers… are the very ones supporting his position in this thread. Well done, Nick.

    How so, Sal? Which papers from that conference, specifically, support Nick’s position in this thread, and how? All of them? Most of them? One of them?

  63. 63
    Joe says:

    Larry Moran said I should rush back here (from his blog) to tell you guys that he is totally ignorant of what ID is and what it argues against.

  64. 64
    bornagain77 says:

    Joe, since Moran cannot see design in this:

    ExPASy – Biochemical Pathways (metabolism) – interactive schematic
    http://web.expasy.org/cgi-bin/.....mbnails.pl

    Then what he said pretty much goes without saying. Moreover, there is really no reasoning with anyone who denies the overwhelming ‘smell’ of design in such complexity (though I admire you tenacity for trying). Especially seeing that Darwinists have not even demonstrated the origin of even one molecular machine by Darwinian processes.

    Michael Behe – Life Reeks Of Design – 2010 – video
    http://www.metacafe.com/watch/5066181

    “There are no detailed Darwinian accounts for the evolution of any fundamental biochemical or cellular system only a variety of wishful speculations. It is remarkable that Darwinism is accepted as a satisfactory explanation of such a vast subject.”
    James Shapiro, molecular biologist, National Review, Sept. 16, 1996

  65. 65
    Joe says:

    Well Larry sez he is going to come down to MA to call me an idiot to my face. So if you have something to say to him you better do it before then.

  66. 66
    scordova says:

    The number of generations for a mutant to fix (if it fixes at all) is approximated as 4 Ne, where Ne is the effective population. Effective population is the segment of the population that is able to reproduce. Now, if the effective population of humans is about 1.5 Billion humans, the time to fixation is 4 x 1.5 billion = 6 billion generations or about 120,000,000,000 years. 😯

    But after 6 billion generations of humans, at a rate of 3.0 x 10^-8 mutations per base pair (bp) per generation, the expected number of mutations is

    6 billion generation x 3.0 x 10^-8 = 180 mutations per base pair

    Which does not make a lot of sense since that means every base will be mutated 180 times! 😯

    Thus for such large populations it is pointless to be talking fixation! In this case the fixation is not the issue, but rather mutation accumulation.

    I covered the accumulation case here.

  67. 67
    Joe says:

    Mr Sal- slight correction to your post:

    The hypothetical number of generations for a neutral mutant to fix (if it fixes at all) is approximated as 4 Ne, where Ne is the effective population.

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