Researchers from Queen Mary University of London, the University of Oxford, and elsewhere describe "genomic turnover" in the descendants of domestic pigs that came to Europe roughly 8,500 years ago with Near Eastern famers. Starting with PCR analyses on mitochondrial and/or nuclear genome sequences from more than 500 archeological pig samples, the team generated 63 ancient nuclear genomes, which were analyzed in a larger set of 2,099 ancient and modern pig samples going back up to 14,000 years from the Near East and Europe. While pigs in Europe from 6,000 to 7,100 years ago had both Near Eastern and European nuclear ancestry, all but 4 percent of the Near Eastern ancestry had dwindled in Europe more recently. "[O]ur results indicate that while pigs were not independently domesticated in Europe," the authors say, "the vast majority of human-mediated selection over the past 5,000 [years] focused on the genomic fraction derived from the European wild boards, and not the fraction that was selected by early Neolithic farmers over the first 2,500 [years] of the domestication process."
An international team led by investigators at the University of São Paulo looks at potential roles for long non-coding RNAs (lncRNAs) in vaccine-induced immunity. After searching for lncRNAs that coincided with immune response and antibody production in available array- or RNA sequencing-based blood transcriptome profiles for 2,059 blood samples from yellow fever or influenza vaccine cohorts, the researchers did RNA sequencing on samples from 26 children who received intranasal live attenuated influenza vaccines, searching for lncRNAs that were differentially expressed post-vaccination. In particular, they pointed to shared vaccine response-related shifts in the B cell expression of FAM30A lncRNA and nearby immunoglobulin genes. "Taken together, our findings reveal the potential roles of lncRNAs in regulating the immune responses to vaccination," the investigators write, noting that "we created an online database that stores all of the results from our meta-analysis."
Japanese researchers explore the signaling pathway consequences of pancreatic ductal adenocarcinoma (PDAC) drivers: namely, mutations in KRAS and TP53. With a series of cell line expression analyses, protein localization experiments, tumor growth assays, and mouse model experiments, the team teased out interactions between the KRAS and TP53 genes, a cancer-promoting pathway that includes ARF6 and AMAP1, and downstream players involved in cell growth, invasion, and immune responses in PDAC. "[W]e demonstrated that the [two] well-known pancreatic driver mutations cooperatively activate a specific signaling pathway that promotes tumor invasion and immune evasion properties," the authors report, arguing that their findings "provide insights into the molecular basis by which malignancies often develop in parallel with oncogenesis and PDAC cell growth, as well as druggable targets for immunotherapies."