In the PNAS Early Edition this week, Harvard University's David Haig discusses the impact of genomic imprinting on human behaviors, specifically related to kinship after the dissolution of a long-term mating bond. "The innate dispositions of children toward parents and sibs are expected to be sensitive to cues of marital stability, and these dispositions may be subject to effects of imprinted genes," Haig says.
The University of Glasgow's Mariola Kurowska-Stolarska and her colleagues this week show that miR-155 is "upregulated in synovial membrane and synovial fluid macrophages from patients with rheumatoid arthritis." In its functional analyses, the team found that "miR-155-deficient mice are resistant to collagen-induced arthritis," and as such, suggest that the microRNA "may be an intriguing therapeutic target" for arthritis.
Johns Hopkins School of Medicine's Sharrol Bachas et al. discuss "structural contributions to multidrug recognition in the multidrug resistance gene regulator BmrR" in a paper published online in advance this week. Using X-ray and solution studies, the authors characterized multidrug binding by the BmrR protein.
Investigators at Brown University this week "present an intuitive strategy for predicting the effect of sequence variation on splicing," based on the fact that the "positional distribution of a splicing element is a signature of its function." The Brown team's method organizes "all possible sequence motifs into clusters based on the genomic profile of their positional distribution around splice sites," it says. In its analysis of human disease alleles, the team identified known splicing units as having "high intra-allelic distances," as well as evidence to suggest that 22 percent of disease alleles "were originally classified as missense mutations." Overall, the authors suggest that "approximately one third of all disease-causing mutations alter pre-mRNA splicing."