In PLOS One, researchers from Estonia, the US, and Canada describe placental gene expression profiles that seem to be associated with complications such as preeclampsia or gestational diabetes during pregnancy. Using array-based approaches to look at the levels of around 47,000 transcripts in placental tissue from early or mid-gestation, the team tracked down more than genes showing transcriptional shifts at mid-gestation. In most cases, they note, the levels of genes with peak expression at mid-gestation decline in placental tissue at late pregnancy. But for women with pregnancy complications, levels of such transcripts tend to remain high, researchers report.
A new study suggests that at least one of the germline SNPs identified in the DNA polymerase beta gene POLB appears to predispose carriers to increased risk of genome instability and, potentially, cancer. As they write in PLOS Genetics, Yale University's Joann Sweasy and her colleagues transformed human and mouse cells with a version of POLB that contains a germline coding SNP called rs3136797. Whereas the POLB product normally has a gap-filling function that contributes to a genome protective process called the base excision repair pathway, the team found that cells challenged with an alkylating agent were prone to single- and double-strand DNA breaks in presence of the rs3136797 POLB variant.
A team from the Public Health Agency of Canada's National Microbiology Laboratory and the University of Manitoba look at the transcriptional patterns in prion infected hippocampal neurons for a PLOS Pathogens study. In hippocampal neurons isolated by laser capture microdissection, the researchers saw gene expression and microRNA patterns that resembled those found during synaptic N-methyl-D-aspartic acid, or NMDA, receptor signaling or following the activation of neuroprotective pathways. "Our findings suggest that prion replication results in the persistent stimulation of a programmed response that is mediated, at least in part, by synaptic NMDA receptor activity that initially promotes cell survival and neurite remodeling," senior author Stephanie Booth and her co-authors say, "However, this response is terminated prior to the onset of clinical symptoms in the infected hippocampus, seemingly pointing to a critical juncture in the disease."