The cholera-causing bacterial species Vibrio cholerae can gain drug resistance via a range of mobile genetic elements, according to researchers in India and the UK. The team assessed resistance or susceptibility to 22 antibiotics in more than 400 V. cholerae clinical isolates, obtained from stool samples for individuals treated for diarrhea in Kolkata or Delhi between 2008 and 2015. From there, the authors dug deeper into multidrug resistant or extensively drug resistant strains with whole-genome sequencing on four of the isolates, representing distinct serotypes and resistance profiles, and did mass spec-based proteomic profiling on one extensively drug resistant V. cholerae isolate. "We show that V. cholerae is evolving continuously by gaining fitness traits through [horizontal gene transfer]," they write.
A Simon Fraser University- and BC Children's Hospital Research Institute-led team investigate troponin I mutations identified in a subset of autopsy-negative "sudden unexpected death of an infant" (SUDI) cases. The researchers focused on 10 SUDI cases marked by the same TNNI1 mutation in a targeted sequencing analysis that profiled more than 70 genes in 191 SUDI cases not be explained by autopsy. Based on findings from their phylogenetic, molecular, and biophysical analyses — along with results from gene editing experiments that introduced the TNNI1 mutation to heart cells produced from human induced pluripotent stem cells — they propose a model in which the troponin I alteration contributes to sudden cardiac death of infants by altering heart function and increasing the risk of arrhythmia.
Researchers from Beijing Normal University, the Chinese Glioma Genome Atlas Network, and elsewhere share findings from a transcriptome analysis of glioma that focused on the tumors marked by genomic instability. Starting with available glioma transcriptome data, the team identified a set of genes that appear to be co-expressed with CDC20 at higher-than-usual levels in tumors with genomic instability — a module containing an AURKA gene that might be targetable by a US Food and Drug Administration-approved inhibitor drug. The set of 139 conserved genes in the CDC20 co-expressed module appears to contribute to processes such as DNA damage response, chromosome segregation, and cell proliferation, the authors note, and results for another 1,305 patients with diffuse glioma suggest that the CDC20 module signature coincided with poor outcomes.