In a previous post, I discussed Michael Behe’s recent paper in Quarterly Review of Biology, “Experimental Evolution, Loss-of-Function Mutations and ‘The First Rule of Adaptive Evolution’,” which reviews much recent work in the field of bacterial evolution. He devotes particular space, however, to the research of Richard Lenski, who has now grown over 50,000 generations of E coli in the lab to study its evolution. Lenski’s work was cited by Richard Dawkins most recent book (The Greatest Show on Earth) as the ultimate refutation of irreducible complexity. Dawkins’ book, however, made a straw man argument by discussing a misguided attack on Lenski’s work by Conservapedia editor Andrew Schalfly, completely ignoring critiques of Lenski’s research by Behe in The Edge of Evolution. Now Dawkins’ book is doubly out-of-date as Behe has published a peer-reviewed article in Quarterly Review of Biology that provides an even deeper assessment of Lenski’s claims.

As evidence that Lenski’s research involved loss of function rather than gain, in one instance of E. coli evolution from Lenski’s research, Behe notes that “the investigators saw that several genes involved in central metabolism were knocked out, as well as some cell wall synthesis genes and several others.” After reviewing the results of Lenski’s research, Behe concludes that the observed adaptive mutations all entail either loss or modification–but not gain–of Functional Coding ElemenTs (FCTs):

The results of future work aside, so far, during the course of the longest, most open-ended, and most extensive laboratory investigation of bacterial evolution, a number of adaptive mutations have been identified that endow the bacterial strain with greater fitness compared to that of the ancestral strain in the particular growth medium. The goal of Lenski’s research was not to analyze adaptive mutations in terms of gain or loss of function, as is the focus here, but rather to address other longstanding evolutionary questions. Nonetheless, all of the mutations identified to date can readily be classified as either modification-of-function or loss-of-FCT. … In the most open-ended laboratory evolution experiment (Lenski 2004), in which no specific selection pressure was intentionally brought to bear, all of the adaptive mutations that have been so far identified have either been loss-of-FCT or modification-of-function mutations, and there is strong reason to believe that most of the modification-of-function mutations diminished protein activity.

(Michael J. Behe, “Experimental Evolution, Loss-of-Function Mutations and ‘The First Rule of Adaptive Evolution’,” Quarterly Review of Biology, Vol. 85(4) (December, 2010).)

Behe Goes Viral
Behe also reviews molecular changes in viruses. Although much work remains to be done towards understanding the molecular mechanisms that underlie virus evolution, Behe argues that there are still few examples of adaptive viral evolution that entailed gain of a new FCT:

Except in cases where specific genetic features were first removed, as well as in the case of antibiotic gene capture by f1, all adaptive mutations in laboratory evolution experiments with viruses seem to be loss-of-FCT or modification-of-function mutations.

Thus Behe found whenever there was a gain-of-function mutation in viruses, it involved “intentional introduction by the investigator.”

After reviewing a number of studies, Behe concludes: “As can be seen, only one of the adaptive mutations from bacteria (Tables 2 and 3) is gain-of-FCT, yet several adaptive mutations from experiments with viruses (Table 4) belong to that class as well.” He asks “Why the difference?” and suggests that in addition to much higher mutation rates in viruses, it might have something to do with the intelligently designed virus experiments mentioned above:

One reason may be that, except for the capture of an antibiotic resistance gene by phage f1, the viral gain-of-FCT mutations all reconstruct functional coded elements that had been deliberately removed from–or rendered inactive in–the ancestral virus, thus restoring pieces of a once integrated system. That is, they began at a point that was known to be able to benefit from a gain-of-FCT mutation.

In another case of viral evolution, Behe noted that “[t]he mutant that achieved the greatest fitness was the one that reverted completely to the wild type sequence.” Such cases are analogous to taking a hiker already on the top of a mountain peak, knocking him down a few feet, and then boasting about his ability to climb to the top of a mountain. In fact, Behe reported that in some studies, if the hiker was knocked too far down the mountain, he was not able to climb back up again:

Considering the time- and population scale constraints of the experiments, it is not surprising that, when large experimental deletions were constructed that removed the coding sequences of whole genes (rather than just frame shift mutations or short control elements), the deleted genes were not restored. Indeed, it was surprising that more modest adaptive gain-of-FCT mutations were not seen either. The removal of T7 ligase resulted in point mutations and deletions in other genes involved in DNA metabolism, which are loss-of-FCT and modification-of-function mutations.

The implication, of course, is that there may be empirically observed limits even to viral evolution.