swamidass
February 20, 2019, 4:02am
11
That is how I understand it too.
The flaw in their argument has been pointed out by @art , and is just as bad a reading of the literature on malaria as the polar bear fiasco. @Art has this one correct, which is why I repeatedly quote him on this (still no response from DI).
The Story On Malaria
As for the specific problems with this study in supporting Behe’s argument, I direct you to two places. First to Larry Moran’s dialogue with Behe, in which his explanation of the science is quite solid: Prof. Behe’s debate with Prof. Moran . I also direct you to @Art hunts article on this Behe and the limits of evolution | The RNA Underworld . You will see that Larry comes to a different conclusion, rightly so. @art ’s article merits some explanation.
Note that Malaria probably requires many more than just two mutations to become resistant. Behe badly misreads the epidemiological data on this. For his argument to work, clinical resistance to malaria must require two and only two mutations. Here is how @art summarizes it:
’ll close this essay by noting one source of error on Behe’s part. As I have discussed, Behe asserts that the probability associated with a “CCC” is 1 in 10^20. Where does this number come from? From footnote 16 in the first excerpt given above – White, N. J. 2004. Antimalarial drug resistance. J. Clin. Invest. 113:1084-92. Here is the actual passage from the review by White that mentions the number 10^20:
“Chloroquine resistance in P. falciparum may be multigenic and is initially conferred by mutations in a gene encoding a transporter (PfCRT) (13). In the presence of PfCRT mutations, mutations in a second transporter (PfMDR1) modulate the level of resistance in vitro, but the role of PfMDR1 mutations in determining the therapeutic response following chloroquine treatment remains unclear (13). At least one other as-yet unidentified gene is thought to be involved. 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. “
Recall that Behe equated one CCC with a double mutation, presumably based on other work showing that two point mutations in the PfCRT gene are associated with durable resistance in the parasite. But White is not talking about double mutations in PfCRT when he tosses out the number 10^20. Rather, he is speculating about the frequency of occurrence of a multigenic trait that involves two or three genes, and more (perhaps many more) than two mutations . In other words, Behe’s use of this citation to argue that the natural frequency of occurrence of a double mutation in PfCRT is 10^20 is inappropriate. This is one reason (not the only reason, but one) why Behe’s claims are so out of touch with reality.
Behe often comes back to this misreading to demonstrate that unguided mutations can’t do much. From the ENV article, see what was written:
Behe is just making the reasonable observation that “none of the mechanisms of EES [Extended Evolutionary Synthesis] proponents were anywhere to be seen” in helping this feature to evolve, because “a couple of classical random point mutations in the gene for a single protein plus run-of-the-mill Darwinian natural selection” were sufficient.
That is a reference to this misreading. He think that CCC is just two mutations, but it is actually many more than this. So it turns out that evolutionary processes (which include more than Darwinian natural selection and the EES) can actually accomplish quite a bit more than he thinks. Not just 2 mutations, but many many more.