New York University School of Medicine's Evgeny Nudler et al. link RNA polymerase backtracking to genome instability in E. coli in Cell this week. In its paper, the NYU team shows that "co-directional collisions between backtracked RNAP [RNA polymerase] and replisome lead to DSBs [double-strand breaks]" in the bacterium. It also shows that "active ribosomes preserve genome integrity" by preventing such backtracking.
Danesh Moazed at Harvard Medical School discusses "mechanisms for the inheritance of chromatin states" in the current issue of Cell. In his paper, Moazed proposes "models for the maintenance of epigenetic information in which DNA silencers or nascent RNA scaffolds act as sensors that work cooperatively with parentally inherited histones to re-establish chromatin states following DNA replication."
Researchers at the University of Brisbane and elsewhere this week report on previously unidentified transcripts in the human mictochondrial transcriptome, which they characterized across multiple cell lines and tissues. "Using directional deep sequencing and parallel analysis of RNA ends, we demonstrate wide variation in mitochondrial transcript abundance and precisely resolve transcript processing and maturation events" through the human mictochondrial transcriptome, the authors write. The team also reports a "global profile of DNA-binding protein occupancy across the mitochondrial genome at single-nucleotide resolution," which they generated using an in vivo DNaseI footprinting technique.
Over in Cell Host & Microbe this week, Harvard Medical School's Matthew Waldor and his colleagues report their use of "massively parallel cDNA sequencing — RNA-seq — techniques to quantitatively catalog the transcriptome of the cholera pathogen, Vibrio cholerae, derived from two animal models of infection." Waldor et al. report finding transcripts deriving from the major known V. cholerae virulence factors were elevated in infected rabbits and mice when compared with laboratory media. "RNA-seq-based transcriptome analysis of pathogens during infection produces a robust, sensitive, and accessible data set for evaluation of regulatory responses driving pathogenesis," the authors write.