The Journal of Eukaryotic Microbiology recently published several papers from a workshop sponsored by the International Society of Protistologists titled “Horizontal Gene Transfer and Phylogenetic Evolution Debunk Intelligent Design.” So here we have a respected scientific society, presumably planning a workshop months in advance, and finally laying out their considered case for why intelligent design fails. As you might imagine, I was most anxious to read about it. Unfortunately, rather than scholarly papers, the manuscripts read like press releases from the National Center for (Darwinian) Science Education. So the introductory essay1 by Avelina Espinosa tells us that ID has “creationist beginnings,” claims that I say “evolution” is “impossible,” and places in my mouth the phrase “design creationism” (I have never uttered that phrase except to disparage it). Blah, blah, blah. About as much scholarship as you’d get from a typical politician.
The first of the full articles2 concerned itself mostly with common descent, which I have always said I think is correct, and which in any case is not an issue of intelligent design. Another article, however, briefly dealt with my case from The Edge of Evolution, that some adaptations are likely to require multiple mutations, and thus be very improbable.* In “Using Protistan Examples to Dispel the Myths of Intelligent Design”3 University of Georgia Professor Mark Farmer and Wadsworth Center Dr. Andrea Habura start off sloppily: “According to Behe (2007), the odds that mutations required to impart chloroquine resistance in Plasmodium could arise naturally are so impossibly long that they lie beyond what he considers ”The Edge of Evolution.'” But the book clearly states that chloroquine resistance in Plasmodium did arise naturally, by Darwinian processes. I go on to argue it took very many malarial parasites to chance upon resistance, and that pointed to a limit for Darwinian evolution for more complex mutations, or for populations with smaller numbers than Plasmodium, but I clearly said the opposite of what Farmer and Habura3 ascribe to me, that chloroquine resistance arose naturally. That doesn’t give a reader confidence that the authors concern themselves much with the details of an argument.
Farmer and Habura think I am wrong that multiple mutations were necessary in the protein PfCRT to confer chloroquine resistance on malaria. They think only one will suffice. What’s more, they claim there are experiments to show that. They cite two papers.34 But neither paper even tries to test whether a single mutation in PfCRT confers chloroquine resistance. Lakshamana et al. (2005) show that if they remove one particular mutation (K76T) from a mutant protein that carried a half dozen or so other mutations (compared to the wild-type protein), the protein no longer confers chloroquine resistance. That experiment shows the K76T is necessary; however, it does not show it is sufficient by itself, as Farmer and Habura thought. The same goes for the second paper. In their methods section Jiang et al (2008) write that “Parasite 106/1K76 [a chloroquine-sensitive strain that does not have the K76T mutation] has six mutations found typically in Southeast Asian CQR parasite … except a key mutation at PfCRT 76 position.”) Thus both these papers show that K76T is necessary, but neither shows it to be sufficient. To do so one would have to test the K76T in the wild-type, unmutated background.
To recap, several years after The Edge of Evolution was published a scientific society held a workshop to demonstrate the book’s errors. Yet they couldn’t even get the book’s argument straight, and the experimental work they cited against my argument is not even pertinent to it. Apparently the design argument drives some scientists so much to distraction that they lose their normally robust powers of reasoning.
*Most of the second paper actually dealt with making a case for macroevolution based on a series of fossil foraminifera. Whether or not one wishes to classify the series as an example of “macroevolution,” the accompanying drawings are not likely to persuade skeptics, and in any event are at the anatomical level rather than the molecular level, where, I have always argued, one must look to determine whether an evolutionary event is feasible by Darwinian processes.
1 Espinosa, A. 2010. Introduction: protistan biology, horizontal gene transfer, and common descent uncover faulty logic in intelligent design. J. Eukaryot. Microbiol. 57:1-2.
2 Paz, Y. M. and Espinosa, A. 2010. Integrating horizontal gene transfer and common descent to depict evolution and contrast it with “common design”. J. Eukaryot. Microbiol. 57:11-18.
3 Farmer, M. A. and Habura, A. 2010. Using protistan examples to dispel the myths of intelligent design. J. Eukaryot. Microbiol. 57:3-10.
4 Lakshmanan, V., Bray, P. G., Verdier-Pinard, D., Johnson, D. J., Horrocks, P., Muhle, R. A., Alakpa, G. E., Hughes, R. H., Ward, S. A., Krogstad, D. J., Sidhu, A. B., and Fidock, D. A. 2005. A critical role for PfCRT K76T in Plasmodium falciparum verapamil-reversible chloroquine resistance. EMBO J. 24:2294-2305.
5 Jiang, H., Patel, J. J., Yi, M., Mu, J., Ding, J., Stephens, R., Cooper, R. A., Ferdig, M. T., and Su, X. Z. 2008. Genome-wide compensatory changes accompany drug- selected mutations in the Plasmodium falciparum crt gene. PLoS. One. 3:e2484.