In this week’s issue of Science, researchers report that RTEL-1 enforces meiotic crossover homeostasis ― specifically, it acts as a regulator of the distance between crossover events on the same chromosome to prevent interference. The authors write that “antirecombinase RTEL-1 is required to prevent excess meiotic COs [crossovers], probably by promoting meiotic synthesis-dependent strand annealing.” The team also suggests that RTEL-1 enforces an additional level of control by promoting non-crossovers.
In an advance, online publication of Science Signaling, a pair of researchers at the University of Rochester and the Massachusetts General Hospital report that stress-activated Cap’n’collar transcription factors, such as Nrf2, defend against oxidative stress and disorders associated with aging in rodent models. The authors write that in humans, polymorphisms which decrease Nrf2 levels are associated with various pathologies. Because the activity of Cnc factors declines in aging organisms, the team suggests the possibility of pharmacological restoration of Nrf2 signaling to prevent and treat age-related diseases.
In this week’s issue of Science Signaling, researchers in the US and the UK demonstrate that the proteomic signature of the ischemic-tolerant ― transcriptionally suppressed ― brain is defined by an increased abundance of transcription-repressing polycomb group proteins. When the team performed knock-down studies of the PcG proteins, they observed induced ischemic tolerance; they write that “PcG proteins are associated with the promoter regions of genes encoding two potassium channel proteins that show decreased abundance in ischemic-tolerant brains.” The authors report a previously undetected neuroprotective mechanism involving proteins in the PcG family as epigenetic mediators.
A research article appearing in Science Translational Medicine this week outlines the work of five researchers at Duke University who propose a “novel paragidm for infectious disease diagnosis.” Aimee Zaas et al. report gene expression signatures in blood that are indicative of candidemia, a common infection, caused most often by Candida albicans. Using a murine model, the team validated a genetic signature known to have associations with host defense against Candida and similar microorganisms.