Lents and Swamidass: Our Questions for Behe’s Darwin Devolves

[swamidass (S. Joshua Swamidass)]

@Dan_Durston

By argument, I’m referring to what appears to be the central thesis of Behe’s book that “devolution” or loss of genetic function in the main result of Darwin’s mechanism.

You are introducing a different argument than the one he first put forward 20 years ago, and then the next one he put forward 10 years go. We are happy to address what you are raising in another thread, however, this does not explain why Behe has in his book:

1. Excluded the many valid counter examples and arguments against his (falsified) hypothesis that “IC1 systems cannot evolve” (Black Box) I’d encourage you catch up a bit by reading this brief summary: Which Irreducible Complexity?

2. Equivocates Darwinism (i.e. positive driven change) with modern evolutionary science.

3. Did not correct his misreading of a quote about the malaria complexity cluster (IC2), which is the central validation he points to in his last book, even as he draws on it now to make his case (Edge of Evolution).

@Art

Here is the part of White’s review from which Behe pulled the value 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.

The bottom line is that the number bandied about by Behe et al. (1 in 10^20) is not really representative of the frequency of the CCC he discusses in the EoE.

As for the new argument you are offering, we can discuss that in another thread. We will find that there are many mechanisms that add genetic information to genomes quite easily. That, however, is a story for another thread.