Of the many scientists who are trying to understand evolution, Richard Lenski stands out for his experimental approach. He has maintained stocks of E. coli growing under stressful conditions for over 40,000 generations.During that time, the cells have been forced to adapt to conditions of low carbon source (glucose) and Lenski's group has been tracking the mutations that arise. In the past, they have done a heroic job of identifying new mutations but that job has become much easier with new technology. Now that rapid genome sequencing is possible it becomes feasible to sequence the genomes of bacteria that were preserved from earlier generations and determine every single mutation that arose.
Barrick et al. (2009) have published the result from just such an experiment. They sequenced the genomes of the original, ancestral, strain and samples of a single lineage from 2,000, 5,000, 10,000, 15,000 20,000 and 40,000 generations.
This information can address a number if issues as they explain in the introduction to their paper.
Genomic changes underlie evolutionary adaptation, but mutations—even those substituted (fixed) in evolving populations—are not necessarily beneficial.Variation in the rate of genomic evolution is also subject to many influences and complications.On the one hand, theory predicts that neutral mutations should accumulate by drift at a uniform rate, albeit stochastically, provided the mutation rate is constant. On the other hand, rates of substitution of beneficial and deleterious mutations depend on selection, and hence the environment, as well as on population size and structure. Moreover, the relative proportions of substitutions that are neutral, deleterious and beneficial are usually difficult to infer given imperfect knowledge of any organism’s genetics and ecology, in the past as well as in the present.At 20K generations, there were 29 single nucleotide polymorphisms (SNP) and 16 deletions, insertions, and chromosomal rearrangements (DIP) for a total of 45 different events (see figure). Not all of these contributed to adaptation and the rapid growth phenotype but many of them did. Some were mutations that inactivated a gene and some were amino acid substitutions that change activity of an enzyme.
Experiments with tractable model organisms evolving in controlled laboratory environments minimize many of these complications and uncertainties15,16. Moreover, new methods have made it feasible to sequence complete genomes from evolution experiments with bacteria. To date, such analyses have focused on finding the mutations responsible for particular adaptations. However, the application of comparative genome sequencing to experimental evolution studies also offers the opportunity to address major conceptual issues, including whether the dynamics of genomic and adaptive evolution are coupled very tightly or only loosely.
The authors do not report the distribution of beneficial vs neutral mutations but the data suggests that most of the 45 mutations were beneficial. The authors do not tell us how many of these beneficial mutations destroyed the activity of a gene and how many just changed the activity of a gene product but it looks like there were about equal numbers of both kinds of mutations.
Much of the paper is about adaptive vs. non-adaptive mutations. At 40,000 generations there were 627 SNP and 26 DIP mutations. The increase was due, in part, to an increase in mutation rate because of a mutation in the mutT gene. One might expect that the initial adaptation would result in selection for beneficial alleles and that neutral alleles would accumulate by random genetic drift in subsequent generations (i.e. from 20K generations to 40K generations). This is probably what happened from 20K generations to 40K generations
In the first 20K generations the strain adapted rapidly to the low glucose concentration and from then on its rate of growth under these conditions increased more slowly. This could also be explained by the initial fixation of adaptive mutations followed by fixation of non-adaptive, neutral, alleles. The authors argue convincingly that this didn't happen. Instead, almost all of the first 45 mutations were probably adaptive. Presumably, the mutations that arose later on (between 10K and 20K generations) were much less beneficial (lower selection coefficient) than the ones that first appeared in the population. This is the interesting, and controversial, part of the paper.
This is a paper that the IDiots can't ignore because it's all about evidence for evolution. It doesn't come as a big surprise that Michael Behe already has a poting on the DISCO website: New Work by Richard Lenski.
There was a time a few years ago when you could predict that the IDiots would try to discredit such a paper. The new strategy seems to be the opposite. They agree with the conclusions and offer them as support for Intelligent Design Creationism.
Here's the latest example from Behe's posting.
Despite his understandable desire to spin the results his way, Lenski’s decades-long work lines up wonderfully with what an ID person would expect — in a huge number of tries, one sees minor changes, mostly degradative, and no new complex systems. So much for the power of random mutation and natural selection. For his work in this area we should be very grateful. It gives us solid results to point to, rather than having to debate speculative scenarios.I don't think I need to comment on such stupidity.
Barrick, J.E., Yu, D.S., Yoon, S.H., Jeong, H., Oh, T,K., Schneider, D., Lenski, R.E., and Kim, J.F. (2009) Genome evolution and adaptation in a long-term experiment with Escherichia coli. Nature Oct 18. [Epub ahead of print] [PubMed] [doi: 10.1038/nature08480]
