Connection Between Epigenome, Selective Mutability, Evolution, and Human Disease
Li, Harris et al., PLoS Genetics
Researchers at the Baylor College of Medicine and elsewhere propose a "connection between the epigenome, selective mutability, evolution, and human disease" based on the findings of their study on associations of structural mutability with germline DNA methylation and with non-allelic homologous recombination mediated by low-copy repeats. "Combined evidence from four human sperm methylome maps, human genome evolution, structural polymorphisms in the human population, and previous genomic and disease studies consistently points to a strong association of germline hypomethylation and genomic instability," the Baylor-led team writes.
Genomes, Evolution, and the K-T Boundary
Adaptive Complexity's Michael White points out a new journal, called Genome Biology and Evolution. The journal editors say in an introduction that "advances in genomic technologies are revolutionizing our perspectives on evolution once again" and that "GBE aims to nurture the highest standard of evolutionary genomic research, with the help of the molecular evolutionary and population genetic expertise." White also says to take a look at one of the journal's first papers, from Indiana University's Michael Lynch. That paper says that there were "widespread reductions in genome size" in mammalian lineages after the Cretaceous–Tertiary boundary, though "there is no evidence for such changes in other vertebrate, invertebrate, or land plant lineage."