In the early, online edition of the Proceedings of the National Academy of Sciences, University of Washington researchers describe interactions between variants in the catechol-O-methyltransferase gene COMT, the brain's white matter properties, and second language immersion in adults. The team performed brain scans over two weeks in dozens of Chinese students shortly after arriving at the University of Washington, comparing the genotypes and so-called white matter fiber tract properties over time in individuals who did or did not enroll in an intensive English language-learning program. Along with changes in white matter properties detected in a learning-related brain region as immersion progressed, the investigators identified variants in COMT that were associated with the extent of structural shifts, study authors say, pointing to learning-linked brain-gene interactions.
A University of Illinois at Urbana-Champaign team tracks real-time transposable element excision activity in individual Escherichia coli cells containing fluorescent reporters and the bacterial IS608 transposable element system. Based on the excision events they detected in these cells, the researchers saw shifts in transposable element activity over different stages of the bacterial cell development as well as variability in activity related to strain background and transposable element orientation. "These direct observations demonstrate that real-time live-cell imaging of evolution at the molecular and individual event level is a powerful tool for the exploration of genome plasticity in stressed cells," they write.
Finally, researchers from the University of Oxford and elsewhere explore the functions of the folliculin-interacting protein-coding gene Fnip1 in mice, following from past studies describing a role for folliculin itself in tumor suppression. In mouse models with loss-of-function Fnip1 mutations, the team detected a range of phenotypic effects, ranging from B-cell deficiency to cardiomyopathy — symptoms resembling those reported in humans with gain of function mutations in the AMP-activated protein kinase gene AMPK, which interacts with a complex comprised of folliculin and folliculin-interacting proteins.