In the early, online edition of the Proceeding of the National Academy of Sciences, researchers from Sweden, Canada, and the US explore genetic patterns associated with adaptive evolution in Atlantic herring. The team re-sequenced the genomes of 40 to 50 fish apiece from half a dozen Atlantic herring population at sites in the North Atlantic. By comparing these genomes with pooled sequences for 19 North East Atlantic or Baltic Sea herring populations and one Pacific population, the investigators saw relatively little genetic differentiation from one Atlantic Ocean site to the next, though they were able to pick out loci with ties to spawning time that appear to have contributed to parallel adaptation in herring populations in the Atlantic and Baltic Sea.
A team from the University of Illinois, Urbana-Champaign, the University of Chicago, and elsewhere take a look at the ancestry of ancient individuals populating coastal communities on the Pacific Northwest. The researchers began by sequencing nuclear and mitochondrial genomes for an individual from southeastern Alaska whose remains are believed to be roughly 10,300 years old. Along with lower-coverage sequences for three individuals with 1,750-year-old to 6,075-year-old samples from British Columbia, the ancient Alaskan individual's sequences suggested that ancient coastal populations in the Pacific Northwest are likely part of a genetically continuous group with ancestry stretching back to structured populations from the late Pleistocene.
Finally, investigators from the Whitehead Institute for Biomedical Research, the Massachusetts Institute of Technology and other centers in Massachusetts point to a role for the SMARCE1 gene as a key contributor to invasive progression in early-stage ductal carcinoma in situ, a condition that can remain benign or progress to invasive breast cancer. Through a search for transcriptional regulators related to the hundreds of genes that are known to show enhanced expression during progression from ductal carcinoma in situ to invasive cancer, the team suspected that SMARCE1 may regulate an invasiveness-related module — a notion supported by its follow-up functional experiments in cell lines, patient tissue samples, and mouse models.