The current issue of Science carries a four-page panegyric (Pennisi 2013) highlighting the career of Richard Lenski on the occasion of the 25th anniversary of the beginning of his long-term evolution experiment. In 1988 Lenski started what then seemed a slightly wacky project — to let cultures of the bacterium Eschericia coli grow continuously under his watchful gaze in his lab at Michigan State University. Every day he or one of a parade of grad students and postdocs would transfer a small portion of the culture into fresh media in a new test tube, allowing the bacteria to grow 6-7 generations per day. Twenty-five years later the culture — a cumulative total of trillions of cells — has been going for an astounding 58,000 generations and counting. As the article points out, that’s equivalent to a million years in the lineage of a large animal such as humans. Combined with an ability to track down the exact identities of bacterial mutations at the DNA level, that makes Lenski’s project the best, most detailed source of information on evolutionary processes available anywhere, dwarfing rival lab projects and swamping field studies. That’s an achievement well worth celebrating.

Still, the important question to ask is, what exactly has this venerable project shown us about evolution? The study has addressed some narrow points of peculiar interest to evolutionary population geneticists, but for proponents of intelligent design the bottom line is that the great majority of even beneficial mutations have turned out to be due to the breaking, degrading, or minor tweaking of pre-existing genes or regulatory regions (Behe 2010). There have been no mutations or series of mutations identified that appear to be on their way to constructing elegant new molecular machinery of the kind that fills every cell. For example, the genes making the bacterial flagellum are consistently turned off by a beneficial mutation (apparently it saves cells energy used in constructing flagella). The suite of genes used to make the sugar ribose is the uniform target of a destructive mutation, which somehow helps the bacterium grow more quickly in the laboratory. Degrading a host of other genes leads to beneficial effects, too.

The Science story references a new paper from Lenski’s lab (Wiser et al. 2013) showing that the bacterial strain continues to improve its growth rate. The chief talking point of the paper is that the rate of improvement follows a curve that will not max out — improvements would continue indefinitely, although at an ever-slowing rate. The natures of the newer beneficial mutations, however, are not reported — whether they, too, are degradative changes, or minor, sideways changes, or truly constructive changes. (I know which way I’ll bet….)

In one supplementary figure the authors show that the increasing growth rate is built on some previously known, beneficial-yet-degradative mutations. Earlier this year Lenski’s lab (Wielgoss et al. 2013) identified a mutation that built on a previous mutation, too, which may prefigure what kind of changes the unidentified mutations in the current paper will turn out to be. Over the course of the project several of the dozen separate strains developed what is called a “mutator” phenotype. In English, that means that the cell’s ability to faithfully copy its DNA is degraded, and its mutation rate has increased some 150-fold. As Lenski’s work showed, that’s due to a mutation (dubbed mutT) that degrades an enzyme that rids the cell of damaged guanine nucleotides, preventing their misincorporation into DNA. Loss of function of a second enzyme (MutY), which removes mispaired bases from DNA, also increases the mutation rate when it occurs by itself. However, when the two mutations, mutT and mutY, occur together, the mutation rate decreases by half of what it is in the presence of mutT alone — that is, it is 75-fold greater than the unmutated case.

Lenski is an optimistic man, and always accentuates the positive. In the paper on mutT and mutY, the stress is on how the bacterium has improved with the second mutation. Heavily unemphasized is the ominous fact that one loss of function mutation is “improved” by another loss of function mutation — by degrading a second gene. Anyone who is interested in long-term evolution should see this as a baleful portent for any theory of evolution that relies exclusively on blind, undirected processes.

References

Pennisi, E. 2013. The man who bottled evolution. Science 342:790-793.

Behe, M.J. 2010. Experimental Evolution, Loss-of-function Mutations, and “The First Rule of Adaptive Evolution”. Q. Rev. Biol. 85:1-27.

Wiser, M.J., Ribeck, N., and Lenski, R.E. 2013. Long-Term Dynamics of Adaptation in Asexual Populations. Science, [Epub ahead of print].

Wielgoss, S., Barrick, J.E., Tenaillon, O., Wiser, M.J., Dittmar, W.J., Cruveiller, S., Chane-Woon-Ming, B., Medigue, C., Lenski, R.E., and Schneider, D. 2013. Mutation rate dynamics in a bacterial population reflect tension between adaptation and genetic load. Proc. Natl. Acad. Sci. U. S. A 110:222-227.

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