In a Cell paper published online in advance this week, an international team led by investigators at Children's Hospital Boston shows that "the RNA exosome targets the AID [activation-induced cytidine deaminase ] … to both strands of transcribed duplex DNA substrates." More specifically, the authors write, the RNA exosome "accumulates on IgH switch regions in an AID-dependent fashion," a process that is "required for optimal" class switch recombination.
In the most recent issue of Cell, Penn State's Zhenhai Zhang and Franklin Pugh present methods to "detect nucleosome positioning and occupancy levels" with ChIP-seq. In addition, Zhang and Pugh discuss the challenges that biologists and bioinformaticians face in "converting the sequence information into knowledge about chromatin."
Researchers at the Broad Institute report in the current issue of Cell Stem Cell that the expression of reprogramming factors sets off "widespread targeted chromatin remodeling." During reprogramming, Richard Koche et al. witnessed "rapid, genome-wide changes in the euchromatic histone modification, H3K4me2, at more than a thousand loci including large subsets of pluripotency-related or developmentally regulated gene promoters and enhancers." This and other "chromatin regulatory events precede transcriptional changes within the corresponding loci," the authors write.
In the current Cell Host & Microbe, investigators at the National Taiwan University report their use of knockdown and ectopic expression experiments to describe a "mechanism whereby miR-141 induced upon enterovirus infection targets the cap-dependent translation initiation factor, eIF4E, for shutoff of host protein synthesis." The team reports that miR-141 knockdown "reduces viral propagation," while ectopic expression of the miRNA "promotes the switch from cap-dependent to cap-independent translation." Further, it shows that the transcription factor EGR1 plays a role in "miR-141 induction in response to enterovirus infection."