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Ken Miller, the honest Darwinist

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Ken Miller just published a review of Michael Behe’s book, Edge of Evolution. Here is Miller at his best:

but Behe has built his entire thesis on this error. Telling his readers that the production of so much as a single new protein-to-protein binding site is “beyond the edge of evolution”, he proclaims darwinian evolution to be a hopeless failure. Apparently he has not followed recent studies exploring the evolution of hormone-receptor complexes by sequential mutations (Science 312, 97–101; 2006),

Ken Miller
Falling over the edge

Miller falsely accuses Behe of not following the Science (2006) paper, yet it’s hard to imagine that Miller missed the widely available public response by Behe of that very study. How could Miller accuse Behe of not following the study, when Behe said:

The study by Bridgham et al (2006) published in the April 7 issue of Science is the lamest attempt yet — and perhaps the lamest attempt that’s even possible — to deflect the problem that irreducible complexity poses for Darwinism
….

The fact that such very modest results are ballyhooed owes more, I strongly suspect, to the antipathy that many scientists feel toward ID than to the intrinsic value of the experiment itself.

In conclusion, the results (and even the imagined-but-problematic scenario) are well within what an ID proponent already would think Darwinian processes could do, so they won’t affect our evaluation of the science. But it’s nice to know that Science magazine is thinking about us!

Michael Behe
The Lamest Attempt Yet to Answer the Challenge Irreducible Complexity,

Despite Behe’s public and widely available commentary on this study, Miller falsely accuses Behe of not following it. Miller asserts boldly, “Apparently he [Behe] has not followed recent studies exploring the evolution of hormone-receptor complexes by sequential mutations (Science 312, 97–101; 2006)“.

I get it, Miller didn’t realize Behe has indeed followed this study and that Behe has even publicly commented on the Discovery Institute’s website. Miller couldn’t possibly have been so dastardly as to actually know Behe published responses to the study, and then falsely accuse Behe of not following the study.

Miller couldn’t possibly be that dastardly. We can therefore attribute it to Miller’s ignorance and simply presume, even though Miller has been obsessed by ID activities, he missed Behe response on the DI website. That can only be the explanation since Miller, being the honest Darwinist he is, can’t possibly do such a dastardly thing. We must chalk this up to his honest ignorance.

[UPDATE:

I found more examples of Ken’s Honesty:

1. Miller falsely insinuates Behe waves away “evidence”

2. Miller’s case against a non-220 CQRs self-destructs by the very paper he cites against Behe

3. Ken Miller needs to know 2004 does not equal 2005

4. Ken Miller reapeats the same misrepresentation he made under oath in Dover

]

Notes:

1. Ken Miller is the guy who has taken various bruisings from scientific evidence and continues his misrepresentations and story telling as he did under oath in the Dover trial. [See: Ken Miller may face more embarrassing facts, Behe’s DBB vindicated and Ken Miller caught making factually incorrect statements under oath]

2. Miller has not (to my knowledge) retracted yet another misrepresentation he made of Behe some time back.

Mike Gene observes in 9+2 = Straw:

In his book, Finding Darwin’s God, Miller finds himself “amused” at Behe’s argument regarding the eukaryotic flagellum, adding, “A phone call to any biologist who had ever actually studied cilia and flagella would have told Behe that he’s wrong in his contention that the 9+2 structure is the only way to make a working cilium or flagellum.” (p.141).
….
But I can’t find where Behe ever raised this contention.
….
what is annoying is that Miller uses this misrepresentation as part of a carefully crafted ad hominem. He begins with “amusement” that leads up to his “A phone call to any biologist” schtick.

Mike Gene

Comments
Art2
I’m wondering - is Behe using the review by White to argue that the frequency of occurrence of a double mutation is 1 in 10^20? Am I reading all of this - the discussion here, as well as EoE - correctly?
White derives the number by dividing the number of times de novo resistance has occurred by the population of the plasmodium under selective pressure of chloroquine resistance. It is a very simple and straight forward scientific observation that only those with a deep emotional commitment to Darwinism have trouble grasping.Jehu
July 1, 2007
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I'm wondering - is Behe using the review by White to argue that the frequency of occurrence of a double mutation is 1 in 10^20? Am I reading all of this - the discussion here, as well as EoE - correctly?Art2
July 1, 2007
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jerry, That's simply not true. There have been numbers of lab experiments which have (in a lab environment) created new alleles. Likewise there are numbers of "field" experiments where the only sensible conclusion is that a new allele has been created. For instance, a mutation in the MSTN gene was recently discovered to produce a strain of fast whippets. This is a new allele which does not exist in wolves or other dog breeds, but makes whippets who carry it run faster. It has arisen naturally via a deletion event, and been selected for by breeders who like fast dogs. New alleles have been observed and sequenced in lab environments in numbers of species, including mice, S. cerevisiae, and brassica (cabbages) being the ones I've read papers about in the last several months.Patrick Caldon
July 1, 2007
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I would like to see one of Behe’s critics answer this question; if CQR can be achieved by single cumulative mutations, why has it arisen less than ten times in past fifty years?Jehu
July 1, 2007
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JAM, At first I thought you were being incredibly disingenuous but perhaps you have only failed to logically follow the argument. Let me help you. Since your comment at #25 you have taken the erroneous position that Behe claimed that Chloroquine resistance (CQR) requires mutations at K76T and A220S. You have maintained this position even after I showed you that Behe’s statement was not that that CQR requires mutations at K76T and A220S but that mutations at K76T and A220S were “almost always present” in CQR strains of malaria. Sal asked you to produce a quote showing where Behe stated that CQR required mutations at K76T and A220S. In response, at comment #44, you surprisingly claimed to have already posted a quote and cited to pages 59 and 60-61 of The Edge of Evolution. Neither of the Behe quotes that you cite say that CQR requires mutations at K76T and A220S. Here are the quotes for the whole world to see. First from page 59: “Let’s compare the two numbers for the odds of achieving resistance to atovaquone, where just one mutation is needed, versus chloroquine, where (presumably – since if a single mutation could help, chloroquine resistance would originate much more frequently) two are needed. ” And from page 60-61: “The likelihood that Homo sapiens achieved any single mutation of the kind required for malaria to become resistant to chloroquine–not the easiest mutation, to be sure, but still only a shift of two amino acids–the likelihood that such a mutation could arise just once in the entire course of the human lineage in the past ten million years, is minuscule–of the same order as, say, the likelihood of you personally winning the Powerball lottery by buying a single ticket.” Do you see anything in either of those quotes about CQR requiring mutations at K76T and A220S? No. Because Behe never makes the claim. Behe’s position is that CQR requires at least two mutations. Although mutations at K76T and A220S are “almost always present” in CQR strains, Behe does not base his position of CQR requiring at least two mutations on the need for mutations at K76T and A220S but on the fact that CQR resistance arises so rarely. How rarely does CQR arise? Here is a relevant quote from page 59. “ Spontaneous resistance to atovaquone [just one mutation needed] can be found in roughly every third sick person. Spontaneous resistance to chloroquine can be found perhaps in every billionth sick person …” The research backing up Behe’s position is as follows: “Resistance to chloroquine in P. falciparum has arisen spontaneously less than ten times in the past fifty years (14). This suggests that the per-parasite probability of developing resistance de novo is on the order of 1 in 10^20 parasite multiplications. The single point mutations in the gene encoding cytochrome b (cytB), which confer atovaquone resistance, or in the gene encoding dihydrofolate reductase (dhfr), which confer pyrimethamine resistance, have a per-parasite probability of arising de novo of approximately 1 in 10^12 parasite multiplications (5).” N.J. White, Antimalarial Drug Resistance, J. Clin. Invest. 113:1084-1092 (2004). Try to understand this JAM. Behe does not claim CQR requires mutations at K76T and A220S. Behe claims CQR requires two mutations. Behe bases this on the rarity of spontaneous CQR not on the explicit need for mutations at K76T and A220S.Jehu
July 1, 2007
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Jam, Maybe you do not understand the process of Neo Darwinism. It eliminates not creates alleles. So the comments "So why would you expect the fewer number of reproductive events to produce all the variety in mammals."" Jam says "Because evolution predicts mostly dead ends (extinctions). When you look at all the variety in mammals, you’re only looking at the rare successes." I am afraid I don't understand your comment or how it answers my objection. Why should these rare successes produce so much variety in the alleles of mammals especially humans. NS and genetic drift drive the elimination or reduction in the variety of alleles. Mutations that produce changes in the allele structure are relatively rare, that is the theme of Behe's book so where did all the different types of alleles come from? This is one of the fundamental contradictions of NDE.jerry
June 30, 2007
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JAM, is this what you're fixated on? "When chloroquine is no longer used to treat malaria patients in a region, the mutant strain of P. falciparum declines and the original strain makes a comeback, indicating that the mutant is weaker than the original strain in the absence of the toxic chloroquine." pp. 50-51PaV
June 30, 2007
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No, why?JAM
June 30, 2007
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What about all the variety in dog breeds in a short time frame?
Been reading Dawkins, lately? ;)Patrick
June 30, 2007
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Sal: What other claim JAM?
The one I directly quoted, Sal, that spans the break between pages 60 and 61.
Unless you back it up with specific citations you are uninvited to this thread. You’re invited to discuss, you’re not invited to fabricate or insinuate things Behe didn’t say.
I'm not fabricating anything. Behe assumes that two substitutions are required twice on p. 59 as well.
Simultaneoulsy for what? Simultaneously for any CQR to exist at all or just for that particular form of resistance?
For me to answer, you'd have to explain what you mean by "form." CQR is simply an empirical measurement that varies by resistant dose. Or are you using "form" to mean "CQR-resistant allele"?
Behe pointed out that that there could be other forms of resistance. However, he was pointing out why this particularly effective one took so long to happen.
No, he gave the reason why (the relative fitness of mutant and wild-type reverses in the absence of CQ) on pages 50-51 but ignored it in his conclusion. What he doesn't mention, and you need to think about, is that this flip-flop of selection pressure goes on in the mosquito in every infectious cycle, so that the mutants are at a disadvantage. We're only looking at the products in populations after selection, not at the raw production of variation.
Don’t parade the strawman that he excluded other possibilities a priori.
I'm not. He has an interesting technique of mentioning things he later ignores in his calculations and conclusions.
Let me give you one from page 61: Someone might object that, since there are thousands of other proteins in an organism, much other DNA, and many other kinds of mutations than just amino acid changes, aren’t the odds of finding some beneficial complex of mutations much better than the odds of finding just the specific complex of mutations we isolated?
That someone wouldn't be me, and I make my living designing mutations that enable proteins to utilize new substrates that aren't found in nature.
The dual PfCRTA144T and PfCRTL160Y mutations are more remote than a single PfCRT220 mutation.
Yes, but since either of them get us to resistance, we add their probabilities together.
It is not surprising that the 220 arose apparently more frequently in several independent places than the A144T and L160Y.
Since we don't know exactly what any of the substitutions do, we can't look at the products of selection as populations and pretend that we are looking directly at the products of mutation.
Baloney. That’s exactly the point of why it took so long for CQR to emerge.
No, the emergence is the product of selection on heterogeneous populations. Behe explicitly gives the reason on p. 50-51, but then abandons it in his conclusion.
There were not many cumulative paths, because had their been, the resistance would have happened in a flash!
The resistance is a product of intermittent, frequently reversed selection. Remember, in each cycle, the Plasmodium is in a mosquito in the absence of CQ, so the wild-type is favored over the mutant.
You apparently don’t get the logic of the argument.
Sal, I get the logic. My problem is with the assumptions. You are assuming that Plasmodium is asexually reproducing under constant selection favoring the resistant allele, as in the case of E. coli in the presence of an antibiotic. The reality is that Plasmodium is sexually reproducing under selective pressures that literally reverse every couple of weeks. Behe notes that the selective pressure reverses in people without CQ, but apparently doesn't realize that this is the case in mosquitoes, too.
The requirement for a long time for resistance to CQ implies there are few effective cumulative paths.
No, it's a product of reversing fitness landscapes.
You’re equivocating the sense of “we assume that two specific substitutions must occur simultaneously”. There are two senses of this phrase: 1. these two are simultaneously needed for a particular kind of CQR (namely a 76 and 220 form of resistance) 2. these two are simultaneously needed for ANY CQR. You are arguing #2 and Behe is arguing #1.
Which is he assuming in his calculation?
Since Behe is not arguing for a single route to CQR,...
Isn't that implicit in his calculation of 10E-20? If you disagree, please walk me through the calculation.
You fail to grasp that the length of time involved in forming CQR is a measure of the amount of cumulative pathways avaialable.
Sal, the length of time is a measure of the strength of selection on populations. Behe even notes that in the absence of CQ, the wild-type has an advantage over the CQR mutants.
If you assert there are lots of pathways that were accessible, you’ll have to account for why it didn’t happen quickly as opposed to decades.
I'm not asserting that. The constantly reversing selection in each reproductive cycle accounts for the speed.
No it is not, for the reasons Behe outlined. Were that path readily available it would have been found far faster. You fail to grasp the logic.
Again, it's about the underlying assumptions. When you genotype clinical isolates of Plasmodium, you are looking at the products of a mixture of wild-type and mutant plasmodia subjected to a constantly-changing (and even reversing, as Behe himself notes) fitness landscape.JAM
June 30, 2007
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jerry: Thus, the relative lack of response to the sickle cell mutation or other means of fighting the parasite has not produced much. So why would you expect the fewer number of reproductive events to produce all the variety in mammals.
Because evolution predicts mostly dead ends (extinctions). When you look at all the variety in mammals, you're only looking at the rare successes. What about all the variety in dog breeds in a short time frame?
Behe has put into numbers what we all instinctively sense from looking at the evidence. So the quibbling over minor changes in amino acid sites may be another form of bluffing and distracting from the real issues.
Behe made this calculation the foundation of his thesis, so pointing out problems with it is neither quibbling nor bluffing. If they are insignificant, then it seems that you should blast Behe for basing his argument on this estimate. There are many additional real issues, for example Behe's neglect of far more rapid mechanisms of genetic variation, such as recombination. The Plasmodium calculation illustrates that issue, too, since Behe discounts the much more likely model of two independent substitutions being put together by recombination. His calculation assumes asexual reproduction and ignores sexual reproduction.JAM
June 30, 2007
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Thanks for the clarification. With regard to the sequential argument, it is helpful seeing the probability there since the wedge argument here is that CQR is "possible" through sequential changes. Seeing that it doesn't functionally change the underlying probability is helpful, as is the clarification of types of CQR Behe is arguing.rswood
June 30, 2007
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Sal, It wasn't a correction. It was a further clarification, which all of us would do well to keep in mind, since this shoots down the usual arguments from those defending the Modern Synthesis.PaV
June 30, 2007
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Thanks PaV for the correction. Salscordova
June 30, 2007
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"1. these two are simultaneously needed for a particular kind of CQR (namely a 76 and 220 form of resistance)" Would it better to say: 1. these two need to both be present for a particular kind of CQR (namely a 76 and 220 form of resistance) There's confusion here, I think, between "simultaneous" and sequential. If the odds of just "one" needed mutation is 1 in 10^12, and the odds of getting both mutations in one cell at the very same time is 10^20, well, I guess it's not impossible for 10^20 malarial cells to be produced without forming any mutation, and then, all of a sudden, to mutate at both positions in the very same reproductive cycle, but it is much more probable---and experimentally verified---that after 10^12 malarial cells have been produced that one of these cells has "one" of the two needed mutations. Then it is simply a matter of waiting for the second to occur from that cell, which has the odds of 1 in 10^8 (the genome size of Plasmodium). This works out to 1 in 10^20, and, lo and behold, Behe uses someone else's calculations to demonstrate the validity of his thinking: Nicholas White of Mahidol University in Thailand points out that if you muliply the number of parasites ina person who is very ill with malaria times the number of people who get malaria per year times the number of years since the introduction of chloroquine, then you can estimate that the odds of a parasite developing resistance to chloroquine is roughly one in a hundre billion billion. In shorthand scientific notation, that’s one in 10^20. Continuing on, it doesn't matter which of the two mutations occurs first,(with the odds of 1 in 10^12 of occuring---based on studies), but the second will occur with the odds of it occurring being 1 in 10^8 (genome size of Plasmodium), giving a total probability of 1 in 10^20. These are "sequential" mutations; not "simultaneous" mutations. But the cumulative odds are the same; i.e., it doesn't matter if they happen at the same time, or if first there is one, and then the other. But, statistically, one would SUPPOSE that they happened sequentially.PaV
June 30, 2007
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JAM wrote: Yes, that demonstrates that he knows that his hypothetical claim elsewhere in the book is false:
What other claim JAM? Unless you back it up with specific citations you are uninvited to this thread. You're invited to discuss, you're not invited to fabricate or insinuate things Behe didn't say.
JAM wrote: Have you found any data to support Behe’s assertion that both substitutions must occur simultaneously?
Simultaneoulsy for what? Simultaneously for any CQR to exist at all or just for that particular form of resistance? Behe pointed out that that there could be other forms of resistance. However, he was pointing out why this particularly effective one took so long to happen. Don't parade the strawman that he excluded other possibilities a priori. Let me give you one from page 61:
Someone might object that, since there are thousands of other proteins in an organism, much other DNA, and many other kinds of mutations than just amino acid changes, aren't the odds of finding some beneficial complex of mutations much better than the odds of finding just the specific complex of mutations we isolated? No. Many, many other mutations in addition to the ones we discusses have popped up by chance in the vast worldwide malarial pool over the course of a few years. In fact mutations in all of the amino acid position in all of the proteins of malaria--taken both one and two at a time--can be expected to occur by chance during the same stretch of time. And other types of mutations besides just changes in amino acids would also occur (such as insertions, deletions, inversions, gene duplications, mobile DNA transpositions, changes in regulatory regions, and others, perhaps even including whole genome duplication---some of these types of mutations are described in the next chapter). Although some other mutations in some other proteins are thought to contribute to chloroquine resistance, none are nearly as effective as that in PfCRT. That means that of all the possible mutations in all of the different proteins of malaria, only a miniuscule number have the ability to help at all against chlorquine, and only one, PfCRT, is really effective.
The dual PfCRTA144T and PfCRTL160Y mutations are more remote than a single PfCRT220 mutation. It is not surprising that the 220 arose apparently more frequently in several independent places than the A144T and L160Y.
JAM asked: Sal, even if we assume that two specific substitutions must occur simultaneously without any evidence,
Baloney. That's exactly the point of why it took so long for CQR to emerge. There were not many cumulative paths, because had their been, the resistance would have happened in a flash! You apparently don't get the logic of the argument. The requirement for a long time for resistance to CQ implies there are few effective cumulative paths. You're equivocating the sense of "we assume that two specific substitutions must occur simultaneously". There are two senses of this phrase: 1. these two are simultaneously needed for a particular kind of CQR (namely a 76 and 220 form of resistance) 2. these two are simultaneously needed for ANY CQR. You are arguing #2 and Behe is arguing #1.
what does each alternative substitution (including those at the same codon) do to Behe’s probability estimate, even if we assume that they must occur simultaneously?
Since Behe is not arguing for a single route to CQR, it doesn't affect the probability of 76 and 220 resistance. Because, assuming we have something like 76 combined with A144T+L160Y, that is statistically more remote than the 76 and 220 pathway. Therefore appeals to this even more remote path as being substantially helpful in terms of accumulation is illogical. It is not surprising A144T+L160Y appear to be rarer than the single 220 substitution. The fact that A144T+L160Y took time to emerge is suggestive there are not very strong cumulative paths to this form of resistance either. You fail to grasp that the length of time involved in forming CQR is a measure of the amount of cumulative pathways avaialable. If you assert there are lots of pathways that were accessible, you'll have to account for why it didn't happen quickly as opposed to decades.
He [Miller} doesn’t have to insinuate anything. It’s a fact.
No it is not, for the reasons Behe outlined. Were that path readily available it would have been found far faster. You fail to grasp the logic.scordova
June 29, 2007
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I botched the quoting at the end of my comment and repeated myself unnecessarily... He doesn’t have to insinuate anything. It’s a fact.
...therefore there is surely a cumulative,sequential, 1-amino-acid-at-at time route, the Miller has made yet another faux pas. Good for him!
Sal, even if we assume that two specific substitutions must occur simultaneously without any evidence, what does each alternative substitution (including those to different aa residues at the same codon) do to Behe’s probability estimate?JAM
June 29, 2007
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One of the things to keep in mind as part of Behe's premise is that there have been more reproductive events in malaria in the last 1000 or 10,000 years then all the mammal reproductive events in history. Thus, the relative lack of response to the sickle cell mutation or other means of fighting the parasite has not produced much. So why would you expect the fewer number of reproductive events to produce all the variety in mammals. Behe has put into numbers what we all instinctively sense from looking at the evidence. So the quibbling over minor changes in amino acid sites may be another form of bluffing and distracting from the real issues. The real issue is that not much happens when things are left alone to evolve or are threatened with resistance (sickle cell) or annihilation (drugs.)jerry
June 29, 2007
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Jehu: Behe’s argument is primarily about the probabilities of certain adaptations arising, not whether a mutation at A220S is is required for chloroquine resistance.
Behe's probability is explicitly derived from that assumption.
Furthermore, Behe never says that a mutation at 220 is always present in chloroquine resistant malaria. Here is what Behe writes in The Edge of Evolution “ However, the same two amino acid changes are almost always present. – one switch at position number 76 and another at position 220. ”
Yes, that demonstrates that he knows that his hypothetical claim elsewhere in the book is false: “The likelihood that Homo sapiens achieved any single mutation of the kind required for malaria to become resistant to chloroquine–not the easiest mutation, to be sure, but still only a shift of two amino acids...”
Notice the “almost.”
I definitely did. Do you notice that "almost" explicitly contradicts his claim that they are required?
The paper you bring up, where 220 is absent, shows that where there is no mutation at 220 there are two other mutations, A144T and L160Y. These two mutations as a substitute for 220 are less probable than a single mutation at 220 and less common as well. This findingcertainly does not damage Behe’s argument.
It makes his estimate of probability exponentially wrong, so it irreversibly damages his argument. Have you found any data to support Behe's assertion that both substitutions must occur simultaneously? Even if both were required, if that assertion is false, his probability is wrong by many orders of magnitude.
If you are going to try to claim that a single mutation can confer chloroquine resistance then please show some evidence of that and explain why chloroquine resistance so rarely arises independently.
I don't have to claim that a single mutation is sufficient. I only have to show that Behe's assumption that two specific substitutions must occur simultaneously is unsupported to show that Behe's estimate of probability is exponentially wrong.
Given the large populations of Malaria in a single infected human and the large number of humans infected, it seems like the probability of any singe amino acid substitution occurring in a given year is quite good.
First, there aren't large populations of Malaria in anyone, because malaria is a disease. The organism we are discussing is Plasmodium.
Therefore, if chloroquine resistance can be conferred by a single mutation, we should see more novel strains of resistant malaria than we do.
Sorry, but that doesn't cut it. You and Behe are omitting the far more rapid mechanisms of variation from the probability estimate, particularly recombination, and completely ignoring sampling bias. You need to realize that always (not almost always) observing both substitutions is absolutely necessary if Behe's hypothesis is correct, but in no way sufficient evidence to state it as fact, which Behe did. For example, the near-universal presence of at least two substitutions in clinical isolates can be explained by independent occurence of each, coupled with an exponential improvement in resistance for the double mutant. The facts of intense selection coupled with recombination then predict that it will be almost impossible to find a resistant isolate with only one substitution.
JAM: Would you please look at Table 1, and tell me if it shows that that resistant Plasmodium exist that lack either K76T or A220S? Jehu: I looked at the table and I don’t see where the table describes anything of the sort.
Every isolate that has "A" at the eighth position shows that.
The body of the article does talk about A220S being replaced by A144T and L160Y in that P2a and P2b strains but this has already been discussed.
How would that change Behe's probability calculation, and where is the evidence that they must occur simultaneously instead of sequentially? And where is the evidence that isolates with two substitutions were not derived from recombination events?
Sal: But I believe Jehu has shown your argument is a misrepresentation.
I don't think I've misrepresented anything. Jehu only pointed out that Behe contradicted himself in the book, which is pretty damaging to Behe's position, not Miller's.
As long as critics are making well-conceived objections (meaning objections that ID proponents themselves might entertain), then I welcome hearing them on my threads.
You might want to reconsider that definition.
Miller fails to inform us that resistance with mutaion 220 missing are equally challenging to evolve because instead of 1 mutation (for 220), to achieve similar effect, one needs 2 mutations in positions 144 and 160, which would suggest since we are dealing with 2 instead of 1, the situation is even more improbable!
Behe fails to inform us that both substitutions don't have to happen in the same Plasmodium, because of a widely-understood phenomenon called recombination. How does considering recombination numerically change Behe's probability estimate?
Thus it doesn’t help miller’s insinuation of a fast sequential path whatsoever.
Sure it does, especially when one considers recombination. Where is the evidence that the substitutions must occur simultaneously?
The point Behe was trying to illustrate in his book was why it took so long for resistance to emerge was that several of the resistance mechanisms require simultaneous changes to have a significantly selectable effect.
But Behe presented no evidence demonstrating that they must occur simultaneously.
And yes, Behe said, “almost”. For miller to insinuate Behe said “never” is a misrepresentation.
Behe's other statement, that they are required, means that one can never be found without the other. Even if they are, that is not sufficient evidence to claim that they must occur simultaneously.
Right on! If Miller is insinuating that because there are CQR (Chloroquine Resistant Malaria’s) like the Philippine strain that do not have te 220 mutation,
He doesn't have to insinuate anything. It's a fact. therefore there is surely a cumulative,sequential, 1-amino-acid-at-at time route, the Miller has made yet another faux pas. Good for him! Sal, even if we assume that two specific substitutions must occur simultaneously without any evidence, what does each alternative substitution (including those at the same codon) do to Behe's probability estimate, even if we assume that they must occur simultaneously? If you can't find any evidence that they must occur simultaneously, why are you trying to place the evidentiary burden on Miller instead of Behe?JAM
June 29, 2007
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Jerry, Your comment was fine. I always look forward to hearing from you. Salscordova
June 29, 2007
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Jehu astutely observes: If you are going to try to claim that a single mutation can confer chloroquine resistance then please show some evidence of that and explain why chloroquine resistance so rarely arises independently. Given the large populations of Malaria in a single infected human and the large number of humans infected, it seems like the probability of any singe amino acid substitution occurring in a given year is quite good. Therefore, if chloroquine resistance can be conferred by a single mutation, we should see more novel strains of resistant malaria than we do.
Right on! If Miller is insinuating that because there are CQR (Chloroquine Resistant Malaria's) like the Philippine strain that do not have te 220 mutation, therefore there is surely a cumulative,sequential, 1-amino-acid-at-at time route, the Miller has made yet another faux pas. Good for him!scordova
June 29, 2007
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JAM, By the way, welcome to the weblog. That was one of the more well-conceived objections that I've heard so far. But I believe Jehu has shown your argument is a misrepresentation. As long as critics are making well-conceived objections (meaning objections that ID proponents themselves might entertain), then I welcome hearing them on my threads. Miller fails to inform us that resistance with mutaion 220 missing are equally challenging to evolve because instead of 1 mutation (for 220), to achieve similar effect, one needs 2 mutations in positions 144 and 160, which would suggest since we are dealing with 2 instead of 1, the situation is even more improbable! Thus it doesn't help miller's insinuation of a fast sequential path whatsoever. The point Behe was trying to illustrate in his book was why it took so long for resistance to emerge was that several of the resistance mechanisms require simultaneous changes to have a significantly selectable effect. We don't know for sure how many possible routes to Chloroquine resistance there are, we know of a few, but evidentially speaking, there are not many, otherwise Chloroquine (CQ) resistance (R) from scratch would have developed much faster. And yes, Behe said, "almost". For miller to insinuate Behe said "never" is a misrepresentation. PS I bet when Behe gives his comprehensive response, he'll squash those misrepresentations by Miller. Right now Behe is merely throwing up his shield at amazon, the counter strike is yet to come.scordova
June 29, 2007
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JAM
No, all it takes is one exception to show that Behe’s claim that both K76T and A220S are required is false.
Behe’s argument is primarily about the probabilities of certain adaptations arising, not whether a mutation at A220S is is required for chloroquine resistance. Furthermore, Behe never says that a mutation at 220 is always present in chloroquine resistant malaria. Here is what Behe writes in The Edge of Evolution “ However, the same two amino acid changes are almost always present. – one switch at position number 76 and another at position 220. " Notice the “almost.” The paper you bring up, where 220 is absent, shows that where there is no mutation at 220 there are two other mutations, A144T and L160Y. These two mutations as a substitute for 220 are less probable than a single mutation at 220 and less common as well. This findingcertainly does not damage Behe’s argument. If you are going to try to claim that a single mutation can confer chloroquine resistance then please show some evidence of that and explain why chloroquine resistance so rarely arises independently. Given the large populations of Malaria in a single infected human and the large number of humans infected, it seems like the probability of any singe amino acid substitution occurring in a given year is quite good. Therefore, if chloroquine resistance can be conferred by a single mutation, we should see more novel strains of resistant malaria than we do.
I think the problem is that you are looking for quotes, when the evidence that clearly contradicts Behe’s claim is in the data, specifically Table 1 of this paper (free PDF available): Antimicrob Agents Chemother. 2005, 49:2102-5._Origin and dissemination of chloroquine-resistant Plasmodium falciparum with mutant pfcrt alleles in the Philippines._Chen N, Wilson DW, Pasay C, Bell D, Martin LB, Kyle D, Cheng Q. I think that’s why Miller says that Behe waves off the evidence. Would you please look at Table 1, and tell me if it shows that that resistant Plasmodium exist that lack either K76T or A220S?
I looked at the table and I don’t see where the table describes anything of the sort. The body of the article does talk about A220S being replaced by A144T and L160Y in that P2a and P2b strains but this has already been discussed.Jehu
June 29, 2007
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This is a little bit off target since it doesn't involve Miller, but does involve Behe and his new book. There was an article in the NY Times this week that is relevant to Behe's thesis. I am afraid to put the link in this site because it will send the post to the nether world. But go to google news and put in "lenski source:new_york_times" and the article will appear in the search. Behe lists Lenski's work as one of the main sources for his conclusions though you will not get that from the article. It is a fascinating article about the changes in bacteria in 20 years of breeding. It is NDE in action. However, it no ways refutes the basic objection to NDE that it works but only on trivial changes in micro organisms. However, some of the changes that did happen are extremely interestiing. There have been lots of mutations that have affected the organism's ability to thrive. This work should be a future addendum to Behe's book. When questioned by Jason Rosenhouse about future ID research, Behe specifically mentioned Lenski as something that should be carried on. Rosenhouse failed to understand how this would support the ID premise. Sorry Salvador that this is not about Miller but it has relevance to the overall discussions going on. Has Miller or anyone else cited Lenski's work in regards to Behe's book?jerry
June 29, 2007
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Here was Behe calling Miller on some more distortions a while back: A True Acid Test: Response to Ken Millerscordova
June 28, 2007
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Miller have just posted a summary of his review on Amazon.com. It would be nice if someone who can comment on reviews at amazon links to this post.IDist
June 28, 2007
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"Ken Miller, the honest Darwinist"? To me it is more like "Ken Miller, the dishonest Darwinist." Ken Miller is a hypocrite. He was an expert witness for the plaintiffs in both the Kitzmiller v. Dover and Selman v. Cobb County evolution disclaimer cases. He says that his own belief in Darwinism is supported by his religious beliefs, yet he misuses the Constitution's establishment clause to try to suppress the views of critics of Darwinism whose criticisms are often not based by religious beliefs. And I was astonished that the plaintiffs in those two cases had the chutzpah to choose a theistic evolutionist as an expert witness in an establishment clause lawsuit.Larry Fafarman
June 28, 2007
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What we need is a wikipedia for evolution, but an honest one
How about this one: ResearchID.orgEndoplasmicMessenger
June 28, 2007
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Sal: Did Miller forget this study? No, all it takes is one exception to show that Behe's claim that both K76T and A220S are required is false. or even in the paper Miller cites and accuses Behe of waving off: Does Miller accuse Behe of waving the paper off, or of waving off the evidence? mutations K76T and Ala220 Ser (A220S) appear to be the most reliable markers predicting CQ resistance. That's true, but it doesn't support Behe's claim that they are required, much less that they must occur simultaneously: "The likelihood that Homo sapiens achieved any single mutation of the kind required for malaria to become resistant to chloroquine--not the easiest mutation, to be sure, but still only a shift of two amino acids--the likelihood that such a mutation could arise just ?once in the entire course of the human lineage in the past ten million years, is minuscule--of the same order as, say, the likelihood of you personally winning the Powerball lottery by buying a single ticket." I think the problem is that you are looking for quotes, when the evidence that clearly contradicts Behe's claim is in the data, specifically Table 1 of this paper (free PDF available): Antimicrob Agents Chemother. 2005, 49:2102-5. Origin and dissemination of chloroquine-resistant Plasmodium falciparum with mutant pfcrt alleles in the Philippines. Chen N, Wilson DW, Pasay C, Bell D, Martin LB, Kyle D, Cheng Q. I think that's why Miller says that Behe waves off the evidence. Would you please look at Table 1, and tell me if it shows that that resistant Plasmodium exist that lack either K76T or A220S? and the final nail in Miller’s argument: ...they [76 and 220] rarely, if ever, occur alone That contradicts Behe right there. For them to be required, they necessarily must NEVER be found alone, not merely rarely. Even if that were true, that is a mere prediction; it would not be sufficient to conclude that they are both required or that they must occur simultaneously instead of sequentially. PS For the situation where 220 is missing but we still find CQR, see comment on A144T/L160Y But if the substitution at 220 is missing in any case at all, Behe's claim that it is required is false. It looks even worse for Behe because elsewhere in the book, he notes that they are "almost always" present. Almost isn't good enough. Scientific citation is generally about the evidence found in the figures and tables, not quoting.JAM
June 28, 2007
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Regarding Super Monkey Ball evolution.
What I find interesting, is that this argument was not used by any of the major reviewers of Behe’s book, as far as I know. It is just popular among Darwin’s internet fans.
I agree that right now only the bloggers are advocating Super Monkey Ball evolution. However, in the past, Allen Orr has demonstrated that he is at heart a believer in Super Monkey Ball . Here is his quote, Consider fitness functions that are as unsmooth as you like, i.e., rugged ones, having lots of peaks and few long paths up high hills. (These are the best studied of all fitness landscapes.) Now drop many geographically separate populations on these landscapes and let them evolve independently. Each will quickly get stuck atop a nearby peak. You might think then that Dembski's right; we don't get much that's interesting. But now change the environment. This shifts the landscape's topography: a sequence's fitness isn't cast in stone but depends on the environment it finds itself in. Each population may now find it's no longer at the best sequence and so can evolve somewhat even if the new landscape is still rugged. Different populations will go to different sequences as they live in different environments. Now repeat this for 3.5 billion years. Will this process yield interesting products? Will we get different looking beasts, living different kinds of lives? My guess is yes. So Allen Orr's guess is that evolution does in fact play Super Monkey Ball. Of course, I am not aware if Orr has or will review Behe this time around, if he does we will have to see if he brings back Super Monkey Ball.Jehu
June 28, 2007
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