I am pleased to announce that Trends in Ecology and Evolution (TREE) has just put up the article-in-press version of my book review of Michael Behe’s The Edge of Evolution. Here is the reference and link:
The DOI link doesn’t seem to be working just yet, presumably that is temporary. And the other link is one of those nasty superlong ones, so if nothing works, go to the TREE website and click on “Articles in Press” to see it (you will have to have a subscription or university access to get the article; I will provide a partial quote below).
Writing this review was challenging. There are a great many things wrong with Behe’s book, and attempting to hit the most important points effectively, with just 750 words to work with, was quite a challenge. For example, there was no way to fit in anything about HIV, even though some really good points have emerged on that front in the last few months. Thanks to the PT crew for a great many helpful discussions, comments, etc. I also had Cavalier-Smith’s (1997) TREE review of Darwin’s Black Box, literally the article that got me into ID criticism in a serious way, to inspire me (despite some flaws in that review).
I tried to make every word count, so it is hard to pick a summary quote, but here is a bit from the middle:
[Behe] attempts to use the evolution of chloroquine resistance (CQR) in Plasmodium falciparum to establish that the origin of multiprotein complexes requires ID. First, Behe admits that CQR evolves naturally but contends that it requires a highly improbable simultaneous double mutation, occurring in only one in 1020 parasites. Second, he asserts that protein-protein binding sites require several simultaneous point mutations and that their occurrence is, therefore, even less probable than that of the alleged double mutation required for CQR. His last step is to square 1020 to produce 1040, the number of organisms required to evolve two binding sites linking three proteins. Given that fewer organisms than this have existed during the history of the Earth, any complex of three or more proteins is beyond the reach of mutations not guided by ID.
The argument collapses at every step. Behe obtains the crucial 1020 number from an offhand estimate in the literature that considered only the few CQR alleles that have been detected because they have taken over regional populations. What is needed, however, is an estimate of how often any weak-but-selectable CQR originates. A study conducted in an area where CQR is actively evolving  showed that high-level CQR is more complex than just two substitutions but that it is preceded by CQR alleles having fewer substitutions; moreover, Behe’s two mutations do not always co-occur. As a result, CQR is both more complex and vastly more probable than Behe thinks. This sinks his one in 1020 estimate for CQR, in addition to his notion that protein-protein binding sites are more complex and, therefore, less probable than CQR. Behe’s decision to square the probability for two binding sites depends on the assumption that two binding sites would have to evolve at once; however, the assumption is false for the same reasons that his ‘irreducible complexity’ argument failed in the first place [1-3]. The squaring assumption is further contradicted by any experiment that accidentally evolves two proteins binding to different sites on a target protein instead of just one .
1 A. Bottaro et al., Immunology in the spotlight at the Dover ‘Intelligent Design’ trial, Nat. Immunol. 7 (2006), pp. 433–435.
2 M.J. Pallen and N.J. Matzke, From The Origin of Species to the origin of bacterial flagella, Nat. Rev. Microbiol. 4 (2006), pp. 784–790.
3 E.C. Scott and N.J. Matzke, Biological design in science classrooms, Proc. Natl. Acad. Sci. U. S. A. 104 (suppl. 1) (2007), pp. 8669–8676.
4 L.J. Briggs et al., More than one way to build a flagellum: comparative genomics of parasitic protozoa, Curr. Biol. 14 (2004), pp. R611–R612.
5 P. Mittra et al., Progressive increase in point mutations associated with chloroquine resistance in Plasmodium falciparum isolates from India, J. Infect. Dis. 193 (2006), pp. 1304–1312.
6 V.A. Petrenko et al., Alpha-helically constrained phage display library, Protein Eng. 15 (2002), pp. 943–950.