Lenski’s the guy who studied all those generations of E. Coli bacteria, and discovered that over many thousands of generations, there were very few beneficial mutations. (Darwinism depends, not on mutations as such but on mutations that benefit the organism.) Recently, his work was the subject of an item, “Evolvability, observed” by Jef Akst (The Scientist, 17th March 2011 ), where we learn
Natural selection picks the most well adapted organisms to survive and reproduce. But what if the most beneficial mutations in the short term meant less room for adaptation in the future?[ … ]
Researchers at Michigan State University and the University of Houston in Texas took advantage of a long-term evolution experiment on Escherichia coli that’s been running for more than 50,000 generations. Characterizing archived strains from 500, 1000, and 1500 generations, the team identified two beneficial mutations that arose in some strains prior to 500 generations and eventually spread through the entire population. The researchers dubbed the strains that carried these mutations at 500 generations the eventual winners (EWs) and those lacking the mutations the eventual losers (ELs).
Andrew J. Fabich at Tennessee Temple University, who knows somewhat of bacteria, writes to say that none of the stuff about them is any big surprise,
Having read the paper, I’m impressed at the magnitude of the research, but not the conclusions. Wood et al. identified a spoT mutation in E. coli as what made his “Eventually Wins” (EW) strains less fit for competition. That’s a no-brainer as spoT mutations studied as much as possible in an isolated background (that of a relA mutant) are always sick. I am not surprised that they identified a gene that made the strain weaker, despite its earlier chances for success. Whenever you mess with the translation machinery and, specifically, the stringent response, you’re setting yourself up for failure. It would’ve been more interesting to see a proper control experiment done in which the spoT mutation was introduced at the beginning of the long-term evolution experiment rather than identified at the very end. This has philosophical implications that Lenski thinks evolution has a goal in mind (i.e., spoT) rather than being random and without a goal.
Does Lenski really think that, then? All ears.
Incidentally, Fabich advises,
I am at no further risk considering my name is already associated with Intelligent Design and being a dissenter. My dissertation was working on E. coli and I followed Lenski’s work because I followed E. coli adaptation in the intestine (rather than the lab) . A fellow graduate student worked directly on the relationship between relA and spoT.