scientific inquiry

Dear Readers, Brown University Professor Kenneth Miller has gotten into a little tiffwith Discovery Institute’s Casey Luskin over what I said/meant about the blood clotting cascade in Darwin’s Black Box.  This is the first of two posts commenting on that. In Chapter 4 of Darwin’s Black Box I first described the clotting cascade and then, in a section called “Similarities and Differences”, analyzed it in terms of irreducible complexity. Near the beginning of that part I had written, “Leaving aside the system before the fork in the pathway, where details are less well known, the blood clotting system fits the definition of irreducible complexity…  The components of the system (beyond the fork in the pathway) are fibrinogen, prothrombin, Stuart factor, and proaccelerin.” Casey Luskin concludes that Read More ›

Dear Readers, An interesting paper has just appeared in the Proceedings of the National Academy of Sciences, “Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli.” (1) It is the “inaugural article” of Richard Lenski, who was recently elected to the National Academy. Lenski, of course, is well known for conducting the longest, most detailed “lab evolution” experiment in history, growing the bacterium E. coli continuously for about twenty years in his Michigan State lab. For the fast-growing bug, that’s over 40,000 generations! I discuss Lenski’s fascinating work in Chapter 7 of The Edge of Evolution, pointing out that all of the beneficial mutations identified from the studies so far seem to have been degradative ones, where functioning genes are knocked out or Read More ›

Dear Readers, An interesting paper appeared recently in the New England Journal of Medicine. (1) The workers there discovered some new mutations which confer some resistance to malaria on human blood cells in the lab. (Their usefulness in nature has not yet been nailed down.) The relevance to my analysis in The Edge of Evolution is that, like other mutations that help with malaria, these mutations, too, are ones which degrade the function of a normally very useful protein, called pyruvate kinase. As the workers note: “[H]eterozygosity for partial or complete loss-of-function alleles . . . may have little negative effect on overall fitness (including transmission of mutant alleles), while providing a modest but significant protective effect against malaria. Although speculative, this situation Read More ›