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This Week in PNAS: May 30, 2017

In the early, online edition of the Proceedings of the National Academy of Sciences, an international team led by investigators in Germany presents findings from a genome and transcriptome sequencing study of two wild tobacco plants, Nicotiana attenuata and N. obtusifolia. The new assemblies — spanning 2.4 billion bases and 1.5 billion bases, respectively — offered a glimpse at the consequences of a whole genome triplication in the Solanaceae plant family lineage, which led to distinct expression patterns for duplicated genes and ballooned transposable element collections in the wild tobacco genomes. The data also provided insights into nicotine biosynthesis, the authors say, noting that the findings "demonstrate the importance of the interplay of gene duplications and transposable element insertions in the evolution of specialized metabolism biosynthetic pathways."

Researchers from the University of Chicago and the University of Helsinki explore the molecular changes associated with mutations to cytochrome c oxidase that alter the way protons interact with a D-channel that translocates them in the resulting protein. For the analysis, the team used a system involving proteins embedded in a lipid bilayer along with so-called multi-scale reactive molecular dynamics simulations, unraveling proton pump impairment mechanisms associated with cytochrome c oxidase mutations. The study "not only provides insight into the decoupling mechanisms of [cytochrome c oxidase] mutants," the authors note, "but also explains how kinetic gating in the D-channel is imperative to achieving high proton-pumping efficiency in the [wild type cytochrome c oxidase]"

Finally, a team from Cincinnati Children's Medical Center, the University of Cincinnati College of Medicine, and elsewhere describe results from a study that involved tinkering with DNA damage response-signaling pathways in antigen-activated lymphocytes as a potential means of tackling immune diseases such as multiple sclerosis in an antigen-specific manner. Reasoning that the rapid cell division undertaken by antigen-activated lymphocyte immune cells may lead to genomic stress, the researchers documented an uptick in DNA damage repair in activated T cells from mice or humans and identified a p53 inhibitor that appeared to staunch pathological T cells in vivo. "We describe a unique strategy for therapeutic immune suppression, relying on targeted manipulation of DNA damage-response signaling, that exploits unique aspects of lymphocyte biology," the researchers say.