I see this response in EVN going right at @swamidass the Christian, not @swamidass the scientist who happens to be Christian. I see this as an attack of @swamidass for attacking a fellow Christian (Behe and DI). This is the problem when faith and science are intermixed. ENV are writing to their Evangelical Christian base with “look how Swamidass the Christian is attacking Behe the Christian” It is Christian dog whistles, just like Deb Haarsma talking about advances in genetics and genetic testing is dog whistle for Evangelistic Christians on Abortion.
Except I didn’t personally attack him, for the record. Moreover I am not arguing for Darwinian evolution. This is something that really does seem to be a slur designed to discredit me.
I’m glad they finally made a substantive response. Let see how things play out from here. I’m looking forward to watching, and responding if need be at a later point.
We are however waiting for a response from Behe.
A few brief remarks about this incredible concession:
-
Good news – I am not longer some “other guy”, at least for the ENV author of this piece.
-
The parts of this essay that relate to my blog post make significant concessions. Thus:
"Here, in defining a CCC, Behe doesn’t specify exactly what is involved in producing it other than some “cluster of mutations.” The details of that ‘cluster’ had not been nailed down by scientific research at the time he wrote The Edge . The key point for Behe’s argument isn’t how a CCC is generated, but that whatever is required to produce a CCC, it apparently takes 1020 trials.”
“Note that Behe’s last sentence there acknowledges that “other mutations” are also involved in producing the resistant strains, but that they play compensatory roles. This is consistent with White’s statement (cited by Swamidass in quoting Hunt) that chloroquine resistance might be multigenic. So Behe didn’t disallow the possibility that other mutations and other genes are involved in a CCC.
Again, Behe makes it clear that a CCC involves a “cluster” of mutations, and is not necessarily limited to mutations only in one “particular protein”:”
Recall that the value of 1 in 10^20 comes from this paragraph:
“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.”
This means that, according to this ENV response, a CCC may involve a cluster of mutations (not just two, but three, four, or many more, presumably), and three (or probably more) separate genes. For example, a CCC might involve nine or more point mutations spread amongst three genes. Moreover, if I read Behe correctly, then these mutations need to be coordinated. Well, if nine coordinated point mutations can be found in a population of 10^20 individuals, I would say that the Edge of Evolution is so far removed from what is accessible to biological populations as to be non-existent. This is significant, to say the least. (An adage about babies and bathwater comes to mind.)
Now, I am going to be tentative in this conclusion going forward, since ENV authors are quite prone to misrepresenting scientific articles (through selective quotation and unwarranted extrapolation). While it might seem unusual that this practice might also apply to their treatment of the ID literature and Behe’s books, it is probably not out of the question. (Recall Matti Leisola’s blatant misrepresentation in his Barnes and Noble review of Behe’s latest book.) So, while I am more than glad to accept this concession and move the overall discussion about protein evolution forward, I will wait until I read the same statements and conclusions (a CCC may involve a cluster of mutations (not just two, but three, four, or many more, presumably), and three (or probably more) separate genes) coming from Behe’s keyboard.
A postscript of sorts - what with all the own goals, I would imagine that the DI’s football squad (if it had one) would be pretty hapless.
What was this?
I agree.
We need to hear a response from Behe to move forward. In a technical discussion like this it is hard to argue by proxy, because we can’t know for sure what Behe is saying or not.
Please convey this to the @discovery_institute.
From a previous thread here on Peaceful Science:
Behe, in ENV:
It has been my experience that one very common way for opponents to try to discredit an argument is to exaggerate it, to ignore distinctions an author makes, and/or to change carefully qualified claims into bizarre absolutes. Why, here’s an example right here:
What Behe is saying is that harming genes is the only way that unguided mutations can ever help an organism.
Matti Leisola, in his review on Barnes and Noble:
Behe introduces new molecular-level facts that sink the Darwinian view of life once and for all: Darwinian mechanism sometimes helps survival of an organism but always by damaging or breaking genes. The conclusion is clear: life is the product of a mind.
Matti Leisola
Isn’t their argument that resistance requires at least 2 mutations for initial “resistance”, and that other mutations are of less consequence? So Behe’s point would be that the really improbable part (requiring the 2 mutations) is that initial resistance, but others that optimise or compensate would be more accessible since they’re directly selectable.
For Behe’s argument to work, there must be at most just 2 rate limiting coordinated mutations for clinical resistance. Let’s not get ahead of ourselves though. Let’s wait for Behe’s comment on the accuracy of that post.
Perhaps, but this is not what the ENV piece is saying.
Moreover, if (as I suspect) Behe is actually claiming that 10^-20 represents the “probability” of arriving at the “improbable part” (two coordinated point mutations), then the article from which he pulled this number does not support his claim. This number factors in at least three different genes, and is not restricted to the initial two point mutations.
My reading of Behe was that he’s using papers like Summers et al. (2014) to conclude that the “improbable part” really is 2 specific point mutations, and after that the optimisation comes easily. If that’s the case, then it doesn’t matter how many genes or mutations are involved in the optimisation process, the estimate from the article of 10^20 is, say, 99% driven by those 2 mutations, and 1% by the other optimising mutations.
That is not the case.
Don’t worry though. Just give Behe time to respond.
My reading of Behe was that he’s using papers like Summers et al. (2014) to conclude that the “improbable part” really is 2 specific point mutations, and after that the optimisation comes easily. If that’s the case, then it doesn’t matter how many genes or mutations are involved in the optimisation process, the estimate from the article of 10^20 is, say, 99% driven by those 2 mutations, and 1% by the other optimising mutations.
Fair enough. What I would say, though, is:
-
EoE was published in 2007, long before Summers et al. came out. In 2007, Behe was saying, quite explicitly, that 1 in 10^20 was the frequency in a “real” population with which the double point mutation arose, hence this is a valid estimate for the frequency of origination of a CCC. (The recent ENV piece notwithstanding, this is the core argument in this book, and what has been asserted by the ID community for more than 11 years.) IIRC, he actually quoted a part of the relevant paragraph from White’s review to support exactly this claim. He conveniently omitted the part that shows that the value of 10^20 actually encompasses much more.
-
Even if “the estimate from the article of 10^20 is, say, 99% driven by those 2 mutations, and 1% by the other optimising mutations”, this makes no sense. How does one divvy up 10^-20 into portions based on their relative contributions to fitness or whatever? What is the evidence that one can do this, or that one’s estimate is even remotely close to what ever metric one is arguing for? In 2007, Behe had no way to address this (AND, I reiterate, in 2007 he intended that this value describe the origination of the two point mutations), and I do not believe Behe has ever offered any sort of sensible approach to this issue.
Behe wrote something of interest in his exchange with Larry Moran:
Behe disallows neutral fixation of mutations. This is one of the main reasons why his calculations are off because he thinks the two mutations leading to resistance have to occur simultaneously or nearly simultaneously. He doesn’t allow for a scenario where a neutral mutation becomes common (>5%) in a population which can then interact with new mutations and produce the beneficial phenotype.
@T_aquaticus and @art, he also does not take into account mutational clusters. The fact that point mutations are clustered drops the wait time for two co-occurring mutations by several orders of magnitude.