Wednesday, October 28, 2009

Genome evolution & speciation

Regular readers will recall my interest in genome evolution, particularly as it relates to the origin of new species (here and here). Two significant papers on this subject are available this week. In the first, Barrick et al. looked at adaptation in a laboratory population of E. coli evolving over 40,000 generations. They sequenced six genomes of E. coli from generations 2,000, 5,000, 10,000, 15,000, 20,000 and 40,000 as well as the ancestral E. coli genome for that population. They discovered a surprisingly high and constant rate of beneficial mutations, only a fraction of which were single nucleotide substitutions. Remarkably, all 26 point mutations found in coding regions were non-synonymous, which suggests that the changes were not just neutral drift. Fourteen of these genes with mutations were sequenced in eleven other 20K-generation populations derived from the same ancestor. They found that only twelve of the fourteen genes modified in their population were also modified in at least one other population. Three genes were modified in all populations tested. It's a great experiment and an amazing result.

Meanwhile, in PLoS Biology, Ferree and Barbash report on a species-specific region of heterochromatin on the X chromosome of the fruitfly Drosophila melanogaster that causes female offspring to die when D. melanogaster males hybridize with D. simulans females. One of the key steps in formation of a new species is reproductive isolation. Now, I realize that very often hybridization and even production of fertile hybrid offspring is possible between otherwise "good" species, but natural hybridization cannot be a widespread phenomenon, or we would not have "good" species at all. In the generation of new species, then, something must happen to prevent the nascent sister species from hybridizing and re-merging into a single species. When I think about the standard creationist explanation of species formation by Mendelian combinations (AKA heterozygous fractionation, AKA the theory of heterozygous creation), this issue of forming reproductive barriers has always bothered me. If it's good for anything (which I doubt), the theory of heterozygous creation seems to be primarily an explanation of where new traits come from. Reproductive isolation is just sort of assumed. My own theory of genomic modularity posits that rearrangements in chromosomal architecture lead to novel phenotypes associated with speciation. Ferree and Barbash's work ties the genomic remodeling by transposable elements (heterochromatin) directly to reproductive isolation. That's pretty exciting.

Barrick et al. 2009. Genome evolution and adaptation in a long-term experiment with Escherichia coli. Nature 461:1243-1247.

Ferree and Barbash. 2009. Species-Specific Heterochromatin Prevents Mitotic Chromosome Segregation to Cause Hybrid Lethality in Drosophila. PLoS Biology 7(10): e1000234. doi:10.1371/journal.pbio.1000234.