I've been meaning to write up my own critique of Michael Behe's latest book The Edge of Evolution but there always appear to be more important things to do. Stephen Matheson at Quintessence of Dust has posted a number of articles on the topic. You can find the links in his latest posting Why I'm not a Behe fan, Part IIB: abusing genetics.
I'm in complete agreement with Stephen on one thing ...
These clarifications are important, because much of the criticism of EoE has been botched significantly. The book is bad, really bad, but it can't be honestly characterized as an anti-evolution argument.Many reviews of The Edge of Evolution are not as good as one might expect from scientists who have read the book.
Stephen Matheson gets the essence of Behe's argument so his review is much better than others. However, I'd like to comment on a few things he says ...
I. Behe's assumption of a particular mutation rate is both absurdly oversimplified and inappropriately extrapolated into the entire tree of life.I don't think this is very important. Behe uses a mutation rate of 10-8 per generation and that's pretty accurate for mammals. A better mutation rate would be 10-10 nucleotides per DNA replication (cell generation) [Mutation Rates]. Yes, it's true that different species have different numbers of cell divisions per generation, so Behe should have mentioned this. Bacteria, for example, have a mutation rate of 10-10 per generation because there's only one cell division per generation. (In mammals there are about 100 cell divisions, hence the mutation rate per generation is 100 times greater.)
The basis of all of Behe's calculations is a mutation rate of 1 in 100 million. This is the estimated rate at which misspelling-type mutation occurs in each generation, averaged over the entire genome, in humans. (The number doesn't consider other types of mutation, now known to be more common than previously thought.) Behe uses this number in all of his (flawed) probability calculations. Even if we knew nothing about mutation rates, the notion of extrapolating from an human (or even mammalian) characteristic to the whole of the biosphere (past and present) is ludicrous enough that it would by itself cast doubt on the credibility of the author.
Stephen argues that mutation rates vary from species to species and over time. I don't think so. I think the rate 10-10 per nucleotide per replication has probably been pretty constant over several billion years and I doubt that it differs very much in different species. It's a property of the DNA replication machinery and that's always been the main source of mutation over the long term.
III. Behe claims that huge population sizes automatically generate more evolutionary opportunity than smaller ones do. This is incorrect.I thought Behe was right about this. There are more mutations, and more variation, in large populations than in small ones. I thought that one of the flaws in Behe's argument is that he doesn't take into account the existence of abundant neutral and nearly-neutral alleles in a large population. Many of these contribute to the double mutations that he requires.
It seems so obvious. More organisms means more mutations means more beneficial mutations means more and faster evolution. It's the kind of obvious, simplistic, intuitive claim that forms the bedrock of any folk science. But it's wrong.
On the contrary, very large population sizes lead to a so-called "speed limit" on adaptation that results from competition among beneficial mutations. The phenomenon is called clonal interference and it's particularly well understood in asexual organisms such as bacteria. The basic idea has been around for decades, but measurement and modeling of the phenomenon has been increasing in the last ten years. A very recent report, the subject of an upcoming post here, showed that the beneficial mutation rate in bacteria is 1000 times higher than previously thought – and the underestimation is due entirely to clonal interference.
The effect is not limited to asexual organisms; in fact, the problem of clonal interference is thought to constitute one of the major driving forces behind the evolutionary development and maintenance of sexual reproduction. The idea is that the genetic shuffling that accompanies sexual reproduction can bring beneficial mutations together and increase the effectiveness of selection.
I'm not familiar with this idea of "clonal interference" that seems to increase the number of beneficial mutations and explains the evolution of sex. It sounds fishy to me but I'll have to read up on it—whenever I find the time. Stephen provides the appropriate references.