In a Nature paper published online in advance this week, investigators at the University of California, Irvine, and the University of Southern California present a "genome-wide analysis of a long-term evolution experiment with Drosophila." The team re-sequenced the genomes of Drosophila populations that have gone through more than 600 generations of artificial selection for accelerated development. The team reports that their data suggest selection via "'incomplete' sweep models, in which mutations have not had enough time to fix, and 'soft' sweep models, in which selection acts on preexisting, common genetic variants." They write that "at least for life history characters such as development time, unconditionally advantageous alleles rarely arise, are associated with small net fitness gains, or cannot fix because selection coefficients change over time."
David Grünwald and Robert Singer at the Albert Einstein College of Medicine in New York describe a method for the "in vivo imaging of labeled endogenous β-actin mRNA during nucleocytoplasmic transport." Specifically, Grünwald and Singer apply a super-registration approach using fluorescence microscopy. "With this method we achieve 20 ms time-precision and at least 26 nm spatial precision, enabling the capture of highly transient interactions in living cells," such as mRNA transport in living cells.
Also in Nature this week, an international research team describes the mechanism through which a thalassaemia patient, treated via lentiviral β-globin gene therapy, is no longer dependent on monthly blood transfusions. "Most of the therapeutic benefit results from a dominant, myeloid-biased cell clone, in which the integrated vector causes transcriptional activation of HMGA2 in erythroid cells with further increased expression of a truncated HMGA2 mRNA insensitive to degradation by let-7 microRNAs," the authors have found. The team suggests that the therapeutic efficacy they've seen with their approach could be a result of the dysregulation of HMGA2 in stem/progenitor cells.
And in Nature Genetics this week, DeCode Genetics' Kari Stefansson and his colleagues show an association between common variants near CAV1 and CAV2 and primary open-angle glaucoma. In their genome-wide association study, the DeCode-led team gentoypes 1,263 affected individuals and 34,877 controls from Iceland; they then replicated the association in smaller sample sets from cohorts across Europe and Asia. "The risk variant identified here is located close to CAV1 and CAV2, both of which are expressed in the trabecular meshwork and retinal ganglion cells that are involved in the pathogenesis of POAG," the authors write. See our sister publication GenomeWeb Daily News' coverage of the study, here.