Editor's Note: Some of the articles described below are not yet available at the PNAS site, but they are scheduled to be posted some time this week.
Using a map-based cloning method, a team from Japan has narrowed in on some of the quantitative trait loci linked to pod shattering in the soybean plant. By characterizing two near-isogenic soybean lines in this manner, the researchers found one particularly tantalizing pod shattering QTL candidate. Their subsequent fine mapping experiments in thousands more soybean plants, together with complementation testing, indicate that the QTL effect at that site involves a gene called PDH1 that codes for a dirigent-like protein regulating a pod wall feature called dehiscing force. Pod shattering resistance appears to occur in soybean plants carrying loss-of-function versions of the gene, the study's authors say, leading to lower seed dispersal and yield loss prior to cultivation.
A University of Illinois at Urbana-Champaign-led team turned to comparative transcriptomics in an effort to understand the neuromolecular mechanisms behind the behavioral changes that occur in mice, stickleback fish, and honey bees that are confronted with intrusion into their territory. The researchers did RNA sequencing on samples taken from multiple brain regions in each type of animal following exposure to an experimental territory intrusion. Compared to control animals that did not experience this threat, the mouse, stickleback, and bee brains showed shifts in similar transcript types, including those coding for components of pathways involved in neurodevelopment, hormone-mediated signal transduction, metabolism, and more.
Researchers from Memorial Sloan-Kettering Cancer Center, Foundation Medicine, and the MD Anderson Cancer Center have profiled mutation patterns in samples from 33 individuals with a form of acute myeloid leukemia that can develop from chronic proliferative blood conditions called myeloproliferative neoplasms. The mutation patterns and frequencies found offered new hints about mutation combinations that can prompt leukemic transformation from MPNs to post-MPN AML, for example — information the team used to test post-MPN AML development and treatment in cell lines and mouse models of the disease. GenomeWeb has more on the study here.