In a paper published online in advance in Science this week, the University of Texas at Austin's Jae Bok Heo and Sibum Sung show that the long intronic non-coding RNA COLDAIR is a critical component for the vernalization-mediated epigenetic repression of the floral repressor FLC in Arabidopsis. COLDAIR, Heo and Sung write, "is required for establishing stable repressive chromatin at FLC through its interaction with [polycomb repressive complex 2]."
Also in this week's Science, an international research team led by investigators at the University of California, San Diego, reports its use of differential epistasis mapping to characterize the interactions among kinases, phosphatases, and transcription factors in yeast cells as they respond to DNA damage. These differential interactions, the team members suggest, paint a more accurate picture than the results obtained from investigations in static conditions. "The data also reveal that protein complexes are generally stable in response to perturbation, but the functional relations between these complexes are substantially reorganized," the authors write. "... Differential networks chart a new type of genetic landscape that is invaluable for mapping cellular responses to stimuli."
A public-private research collaboration between researchers at the Swedish University of Agricultural Sciences and Syngenta Seeds has found that "the regulation of flowering time in beets is controlled by the interplay of two paralogs of the FLOWERING LOCUS T gene in Arabidopsis that have evolved antagonistic functions." In this week's Science, the group reports the roles of BvFT2 and BvFT1 in flowering and vernalization responses in cultivated beets, which differ from the roles these paralogs play in Arabidopsis and cereal crops.
Researchers at the Washington University School of Medicine, along with their collaborators, used BID, BIM, and PUMA triple-knockout mice to ascertain the "essential role[s]" of the proteins encoded by these genes in activating BAX and BAK, which "are required for initiation of apoptosis at the mitochondria." Deletion of these three genes "prevented the homo-oligomerization of BAX and BAK, and thereby cytochrome c-mediated activation of caspases in response to diverse death signals in neurons and T lymphocytes," the authors write. The team shows that members of the BID, BIM, or PUMA protein families directly activate BAX and BAK, a process that's required by many forms of apoptosis.