Response to Critics, Part 2: Sean Carroll

Originally published at Michael Behe's Amazon Blog

Dear Readers,

Yesterday I responded to Jerry Coyne’s review of my new book, The Edge of Evolution.  Today it’s Sean Carroll’s turn.

Sean Carroll in Science

Almost the same day that The Edge of Evolution was officially released Science published a long, lead review by evolutionary developmental biologist Sean Carroll, whose own work I discuss critically in Chapter 9. The review is three parts bluster to one part substance, which at least is more substance than Jerry Coyne’s essay.

Here I’ll ignore the bluster and deal with the substantive points. Carroll first covers his rhetorical bases by warning readers that “Unfortunately, [Behe’s] errors are of a technical nature and will be difficult for lay readers, and even some scientists (those unfamiliar with molecular biology and evolutionary genetics), to detect. Some people will be hoodwinked. My goal here is to point out the critical flaws in Behe’s key arguments and to guide readers toward some references.” So, you see, if Carroll’s reasoning doesn’t sound right, well, maybe that’s because you, dear reader, are too slow to understand him. If that’s the case, you’re supposed to just take his word for it.

Unfortunately, his word is demonstrably questionable. He claims that

Behe’s chief error is minimizing the power of natural selection to act cumulatively… Behe states correctly [my emphasis] that in most species two adaptive mutations occurring instantaneously at two specific sites in one gene are very unlikely and that functional changes in proteins often involve two or more sites. But it is a non sequitur to leap to the conclusion, as Behe does, that such multiple amino acid replacements therefore can’t happen.

But I certainly do not say that multiple amino acid replacements “can’t happen”. A centerpiece of The Edge of Evolution is that it can and did happen. I stress in Chapter 3 that in the case of malarial resistance to chloroquine, multiple necessary mutations did happen in the membrane protein PfCRT. I also of course emphasize that it took a huge population size, one that would not be available to larger organisms. But Carroll seems uninterested in making distinctions.

Carroll cites several instances where multiple changes do accumulate gradually in proteins. (So do I. I discuss gradual evolution of antifreeze resistance, resistance to some insecticides by “tiny, incremental steps — amino acid by amino acid — leading from one biological level to another”, hemoglobin C-Harlem, and other examples, in order to make the critically important distinction between beneficial intermediate mutations and detrimental intermediate ones.) But, as Carroll might say, it is a non sequitur to leap to the conclusion that all biological features therefore can gradually accumulate. Incredibly, he ignores the book’s centerpiece example of chloroquine resistance, where beneficial changes do not accumulate gradually.

As a “second fatal blunder”, he asserts I overlook proteins that bind to “short linear peptide motifs” of two or three amino acids. I’ll get to that in a second. Notice, however, that here he is writing simply of a sub-class of protein binding sites, and never gets around to dealing with the question of how the majority of binding sites, those with interacting folded domains, developed. I assume that’s because he has no answer.

Carroll lets his imagination run wild. He thinks it would be child’s play for random processes to develop binding sites, at least for the sub-category of short peptide motif binding:

Very simple calculations indicate how easily such motifs evolve at random. If one assumes an average length of 400 amino acids for proteins and equal abundance of all amino acids, any given twoamino acid motif is likely to occur at random in every protein in a cell.

Wow, every protein in the cell will have a binding site! Methinks Carroll has just stumbled over an embarrassment of riches. If every protein (or even a large fraction of proteins) had such a binding site, then binding would essentially be non specific. (It would be much like, say, the case of the digestive enzyme trypsin, which binds and cuts proteins wherever there is the amino acid lysine or arginine.) As I make clear in The Edge of Evolution, the problem the cell faces is not just to have protein binding sites (which could simply be large hydrophobic patches), but to bind specifically to the right partner.

In fact, if one takes the trouble to look up the references Carroll cites, one sees that a short amino acid motif is not enough for function in a cell. For example, Budovskaya et el (Proc. Nat. Acad. Sci USA 102, 13933-8, 2005) show that the majority of proteins in the yeast Saccharomyces cerevisiae containing a motif recognized by a particular protein kinase were not phosphorylated by the enzyme. What does that mean? It just means that the simple motifs, while necessary for binding, are not sufficient. Other features of the proteins are necessary, too, features which Sean Carroll ignores.

In his enthusiasm Carroll seems not to have noticed that, as I discuss at great length in my book, no protein binding sites — neither short linear peptide motifs nor any other — developed in a hundred billion billion (1020) malarial cells. Or in HIV. Or E. coli. Or in human defenses against malaria, save that of sickle hemoglobin. Like Coyne, Carroll simply overlooks observational evidence that goes against Darwinian views. In fact, Carroll seems unable to separate Darwinian theory from data. He writes that “what [Behe] alleges to be beyond the limits of Darwinian evolution falls well within its demonstrated [my emphasis] powers”, and “Indeed, it has been demonstrated [my emphasis] that new protein interactions (10) and protein networks (11) can evolve fairly rapidly and are thus well within the limits of evolution.”

Yet if one looks up the papers he cites, one finds no “demonstration” at all. Those papers show, respectively, that: A) different species have different protein binding sites (but, although the authors assume Darwinian processes, they demonstrate nothing about how the sites arose); or B) different species have different protein networks (but, again, the authors demonstrate nothing about how the networks arose). Like Jerry Coyne, Sean Carroll simply begs the question. Like Coyne, Carroll assumes whatever exists in biology arose by Darwinian processes. Apparently Darwinism has eroded Coyne’s and Carroll’s ability to separate data from theory.In fact, the data I cite in The Edge of Evolution is a real demonstration. While we have studied them, in a truly astronomical number of chances, a variety of microbes developed precisely none of the sophisticated cellular mechanisms that Darwinist imaginations ascribe to random mutation and selection. That data demonstrates random mutation doesn’t explain the elegance of cellular systems.

Read Michael Behe’s responses to Jerry Coyne and Michael Ruse.

Michael J. Behe

Senior Fellow, Center for Science and Culture
Michael J. Behe is Professor of Biological Sciences at Lehigh University in Pennsylvania and a Senior Fellow at Discovery Institute’s Center for Science and Culture. He received his Ph.D. in Biochemistry from the University of Pennsylvania in 1978. Behe's current research involves delineation of design and natural selection in protein structures. In his career he has authored over 40 technical papers and three books, Darwin Devolves: The New Science About DNA that Challenges Evolution, Darwin’s Black Box: The Biochemical Challenge to Evolution, and The Edge of Evolution: The Search for the Limits of Darwinism, which argue that living system at the molecular level are best explained as being the result of deliberate intelligent design.