To recap yesterday's post: E. Coli were observed in the lab to evolve a 3-mutation-requiring ability to utilize Citrate for food. The researchers see this as being due mainly to genetic drift: Two of these mutations were random changes that did not effect the fitness of the E. Coli, and they became somewhat prominent in the population. Sort of like having many different color butterflies in a population when no color effects the butterfly's survival.
Michael Behe has given his two cents about this over at his amazon blog. In short, he sees this as being an example of how rare it is for multiple mutations to come together and produce something new. He feels that he has established that multiple mutations must be required to produce much of the complex machinery in the cell. (By the way, PZ Myer's rebuttal to this is also well worth checking out). He also feels that much of the evolution we observe today is destructive rather than constructive.
Let's think about this for a moment: Life began perhaps about 4 billion years ago, single cellular organisms are known from about 3.8 billion years ago, and multicellular organisms are known from about 1.7 billion years ago. Michael Behe stated in his book that the earth hosts about 10^20 bacteria. This is astronomically more bacteria than are observed in the experiment. Two billion years were devoted solely to evolution at the cellular level. We also know that the claim that evolution tends to be destructive is not quite true. Via Mad Mike's blog:
"Research by Dan Andersson and colleagues has demonstrated that following mutations that confer resistance, and that lower growth rates in the absence of antibiotics (the supposed "loss of functional system"), compensatory mutations evolve.
What's a compensatory mutation? A compensatory mutation reduces or eliminates the fitness cost of a mutation (often lower growth rate)--in this case, the original mutation that confers (antibiotic) resistance. For instance, compensatory mutations in the rpsL gene reduced or eliminate the costs of streptomycin resistance in Salmonella typhimurium. More recent work has demonstrated this in other bacteria, and in mouse models."
I recall that Behe mentions in his book something called "C. Harlem". This is a variant of hemoglobin which confers resistance to Malaria but does not have the nasty side effects that Sickle-Cell hemoglobin does. This may be a fairly rare form, but if it was present in the Malaria plagued parts of Africa (Unfortunately it was discovered in Harlem, hence the name), it would most likely spread through the population and replace the sickle cell hemoglobin gene in the gene pool. So sometimes mutations are selected for that provide an advantage (with a hefty cost, mind you) but there are better mutations and compensatory mutations.
And Behe's claim about evolution being unable to account for the complexity of the cell is very, very shaky. The main thesis of "The Edge of Evolution" is that two protein-protein binding sites simply must evolve at the same time in order to produce things like the bacterial flagellum or Cilium. Ian Musgrave has written about some research that shows this claim to be false.
Not to mention the fact that we know the bacterial flagellum is not "unevolvable".