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This Week in PNAS: Apr 7, 2015

In the early, online edition of the Proceedings of the National Academy of Sciences, researchers from the US and Thailand used transposon-mediated mutagenesis sequencing to tally up the genes required for growth by the opportunistic pathogen Pseudomonas aeruginosa in half a dozen different growth conditions. After developing more than a dozen mutant P. aeruginosa pools, they grew the bugs on six types of media — including medium based on cystic fibrosis patient sputum — and used sequencing to narrow in on 352 essential P. aeruginosa genes and almost 200 more genes that were required under particular growth conditions. For instance, the study's author note that "compared with Escherichia coli, P. aeruginosa is highly vulnerable to mutations disrupting central carbon-energy metabolism and reactive oxygen defenses."

A team from the UK, Italy, and the US describe widespread copy number variation within a gene called DMBT1, which codes for a human salivary agglutinin protein that helps cavity-causing bacteria and other microbes stick to the surface of human teeth. Using a quantitative PCR test, the researchers performed a more detailed analysis on copy number gains and losses that had been detected in and around the DMBT1 genome by tiling array comparative genomic hybridization. Their results suggest that the CNV mutation rate is high in the region, with cross-population CNV patterns corresponding with agricultural development in different parts of the world.

Finally, researchers from the University of Utah and elsewhere present a possible role for small, nucleolar RNAs, or snoRNAs, in a mouse metabolic stress response pathway that hinges on the action of an enzyme called protein kinase RNA-activated (PKR), which is also known to respond to immune triggers such as double-stranded viral RNA in other mammals. The team used RNA immunoprecipitation sequencing to identify molecules that interact with wild type or mutant versions of PKR in mouse cells following metabolic stress. The search uncovered an over-representation of snoRNAs, which appeared capable of activating PKR in the group's follow-up experiments.