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This Week in PNAS: Nov 28, 2017

In the early, online edition of Proceedings of the National Academy of Sciences, researchers from Canada and French Polynesia outline efforts to profile epigenetic differences in Coho salmon (Oncorhynchus kisutch) reared in hatcheries relative to wild salmon. The team reasoned that methylation changes might be one reason that hatchery-reared Pacific salmon tend to fare worse fitness-wise than wild salmon stocks. The investigators used reduced-representation bisulfite sequencing to profile genome-wide methylation in dorsal muscle samples from 40 juvenile Coho salmon from two sites in Canada's British Columbia province. Methylation appeared to vary with both geography and rearing environment, the authors note, pointing to captive rearing-related epigenetic shifts as a "potential explanatory mechanism" for fitness dips in hatchery-reared salmon.

A team from the US, Sweden, and Germany consider post-transcriptional messenger RNA alterations, particularly RNA editing, in macrophage immune cells and other cell types. Using PCR-based approaches, the researchers explored these so-called epitranscriptomic patterns in macrophages and other immune cell types. Through a series of follow-up experiments, they teased out APOBEC1 enzyme contributions to RNA editing in bone marrow-derived macrophages, for example, as well as the consequences for gene expression, phagocytosis functions, and other immune processes. The authors note that APOBEC1 editing also appears to prompt a rise in pro-inflammatory monocyte cells, hinting at possible ties to some chronic conditions.

National Cancer Institute researchers explore regulatory factors impacting cytotoxic differentiation by CD8+ T cells in the immune system. When it compared array-based gene expression profiles for T cells that differentiated into cytotoxic effector cells and T cells that did not express cytotoxic genes, the team identified 269 differentially expressed genes. While transcription factors such as Runx3 appeared to prompt expression of the cytotoxic gene set, the authors found evidence for cytotoxic gene repression by the STAT3 and ROR-gamma-t transcription factors, which are also involved in producing a pro-inflammatory IL-17 interleukin. "These results highlight the role of the inflammatory environment on T cell responses," they write, "and have implications for the development of T cell-based immunotherapies."