In Science this week, researchers at the University of California, Los Angeles, and their colleagues report that "Dnmt3a-dependent non-promoter DNA methylation facilitates transcription of neurogenic genes." Specifically, Hao Wu et al. performed a genome-wide analysis of postnatal neural stem cells and found that Dnmt3a "occupies and methylates intergenic regions and gene bodies flanking proximal promoters of a large cohort of transcriptionally permissive genes, many of which encode regulators of neurogenesis."
Investigators at Rockefeller University show that neuron-specific Nova and Fox — a neuronal splicing factor — work in combination to regulate phosphorylation and splicing in the mouse brain. They used "Bayesian networks to probabilistically model diverse data sets and predict the target networks of specific regulators" and identified nearly 700 alternative splicing events directly regulated by Nova.
In a Policy Forum article published in Science this week, Jorge Contreras at Washington University in St. Louis discusses "pre-publication data release, latency, and genome commons." Contreras suggests that "many traditional data-sharing practices were challenged, with significant and lasting effect, during the race to sequence the human genome," and discusses a variety of ways in which data spread to the "commons" can be delayed.
Science Signaling journal associate online editor Annalisa VanHook this week references the Kondo et al. paper, published in Science last week, in which investigators showed that the transcription factor Shavenbaby can be converted from a repressor to an activator in Drosophila. In "Non-coding no more," the editor writes that while "the mechanism by which Pri peptides induce cleavage of Svb has not yet been determined, but the production of small peptides from polycistronic RNAs is a previously unappreciated form of posttranslational regulation that is likely to be widespread throughout eukaryotes."
And Science has posted a corrected version of the Sebastiani et al. paper "Genetic signatures of exceptional longevity in humans," which reflects that the authors are re-analyzing their findings because they were "made aware of an inherent defect in the 610-Quad chip that they used to genotype seven percent of their discovery set," according to a Notice to Readers. For clarity, the Notice continues, Sebastiani et al.'s paper now reads: