In the early, online edition of the Proceedings of the National Academy of Sciences, a Dartmouth team describes apparent ties between genetic variants implicated to obesity and brain responses to food cues. The researchers focused on 78 children with or without FTO genotypes that have been implicated in obesity risk. Using functional and structural magnetic resonance imaging, the investigators tracked nucleus accumbens brain activity in nine- to 12-year-old children as they were exposed to food advertising — an analysis that reportedly pointed to enhanced and more widespread nucleus accumbens activity in the children carrying an obesity-associated version of the FTO gene.
Inhibiting a component of the quorum-sensing system may be a promising approach for diminishing the virulence of "adherent-invasive Escherichia coli" in individuals with inflammatory bowel disease, according to another PNAS study. Researchers from the US, France, and Japan investigated the relationship between an E. coli quorum sensor regulator called QseC and stress-related catecholamine compounds in IBD mouse models using mutant versions of E. coli missing QseC, 16S ribosomal RNA gene sequencing to characterize microbial communities, among other approaches. Without the quorum-sensing gene, they detected diminished mouse colonization by a pathogenic E. coli strain previously implicated in IBD. Likewise, the team found clues that colitis risk might be mitigated by chemically inhibiting QseC in IBD-associated E. coli.
Finally, a Harvard Medical School and Washington University School of Medicine team took a look at the DNA methylation and transcriptional consequences of mutations in the Rett syndrome gene MECP2. By combining DNA methylation, expression, and MeCP2 binding patterns, the researchers found that bases typically bound by MeCP2 show enhanced methylation across the body and surrounding regions of long genes repressed by MeCP2, suggesting that the transcriptional repression is related to the number of methylated MeCP2 binding sites in a given gene. "These findings suggest a model in which MeCP2 tunes gene expression in neurons by binding within the transcribed regions of genes to impede the elongation of RNA polymerase," the authors note.