Monday, August 25, 2008

Stephen Matheson's Critique of Michael Behe's Edge of Evolution

 
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.

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.
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.)

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.

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 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.

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.


4 comments :

  1. The clonal interference idea is recent, but seems to have evidence behind it.

    I really do believe that Behe's "argument" is anti-evolutionist. All of the truly significant changes (as he'd call them) are caused by God, with front-loading, a universe designed to produce the required mutations, or perhaps by continual intervention. The form of evolution is maintained, but the essence is creationist.

    What he seems not to recognize is that, because he has absolutely no means of detecting "design" (but only makes bad calculations where he assumes non-design without reason or good cause), he has absolutely no way of determining where (Darwinian) evolution is taking place, and where "design" steps in. That is to say, he has no demonstrable reason to believe that P. falciparum is evolving due to random mutation and natural selection (plus the rest), and not because of design.

    He has no basis for calculating what evolution can do because he has no independent means for distinguishing between design and evolution.

    Glen Davidson

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  2. Hi Larry--

    Thanks much for the link. Re mutation rates over time, let's see if I can get you on board by explaining why I think the extrapolation is a problem for Behe. The question isn't whether mutation rates were wildly different in the past. It's when. We would postulate that the proofreading machinery – assuming it was assembled through natural processes – arose by the same general mechanisms as every other system in the cellular toolkit. And as you correctly note, that machinery is deeply conserved and therefore ancient.

    But as I'll explain in my final post in the series, this is exactly the evolutionary epoch where Behe's challenge is located. He's already granted that "darwinian" mechanisms account for the diversity of species, and perhaps of families and genera. It is at the assembly of complex machinery, even before the origin of multicellularity, that he is drawing his firmest line. And this means that the proofreading systems are themselves among the machines whose origins he is pretending to explain. At the very least, the wildly complex proofreading systems had to arise in the absence of proofreading systems.

    Regarding clonal interference, you got this part wrong: "that seems to increase the number of beneficial mutations..." When you read up on it, I think you'll see that it makes elegant good sense, and you'll learn that it doesn't "increase" the number of beneficial mutations. On the contrary, it decreases the number of beneficial mutations that can contribute to adaptation, by forcing small-effect beneficial mutations to compete with each other.

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  3. 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.

    I am going to take issue with this statement. While I think this rate has been well documented in logrithmically growing cells (where most studies have been done). Under stress, during growth in a biolfilm, or in stationary phase increased mutation frequencies have been observed, hence the whole field of adaptive mutations. (This is all based on work done with microbes, both bacterial and eukaryotic, but that is where mutation rates were determined anyway.

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  4. The Lorax says,

    I am going to take issue with this statement. While I think this rate has been well documented in logrithmically growing cells (where most studies have been done). Under stress, during growth in a biolfilm, or in stationary phase increased mutation frequencies have been observed, hence the whole field of adaptive mutations.

    Assuming that you are correct, a change in mutation frequency during times of stress isn't likely to have much of an impact over millions of years of evolution. What we know from comparing nucleotide sequences (or amino acid sequences) is that the rate of change (mutation plus fixation) is roughly constant over this time frame.

    That's why there's a molecular clock—the rate of fixation of neutral alleles is equal to the mutation rate.

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