In a study appearing in the early, online edition of the Proceedings of the National Academy of Sciences, Texas-based researchers used a combination of gene expression data, DNA methylation profiles, and methyl-CpG binding protein 2 interaction patterns to study Rett syndrome in a mouse model of the disease. Results from the analysis suggest that MeCP2 not only binds to methylated cytosine bases that neighbor guanine, but also to cytosines that are methylated in a non-CG context. The latter sites appear to accumulate methylation after birth and during nervous system development, the study's authors note, leading to altered expression of genes that are regulated by MeCP2.
Researchers from Woods Hole Oceanographic Institution and elsewhere report on findings from a quantitative metatranscriptomic analysis of metabolic pathways in diatoms sampled off the East Coast in Narragansett Bay between May and June 2012. From the transcript sequences detected in five surface water samples, the team looked at the how distinct nitrogen and phosphorus metabolism pathways varied in relation to one another — information that provided hints about resource use by different diatom species in the region.
Finally, a group from the University of Pennsylvania and the University of California, San Diego explored the mechanisms behind alternative splicing in human T cells — white blood cells that are involved in antigen signaling and other immune functions. With the help of RNA annealing, selection, and ligation sequencing, or RASL-seq, and other approaches in T cells with or without typical levels of a splicing factor called CELF2, the researchers tracked events following T cell signaling. Their results suggest T cells can dial up the CELF2 expression through enhanced transcription of the gene and stability of its messenger RNA, leading to altered splicing of other mRNAs.