In Cell this week, investigators at the Baylor College of Medicine in Houston, Tx., report that the "transcription factor DksA prevents conflicts between DNA replication and transcription machinery." Namely, DksA ensures replication completion in E. coli by "removing transcription roadblocks" like amino acid starvation. "This function of DksA is independent of its transcription initiation activity but requires its less-studied transcription elongation activity," the authors write, adding that transcription elongation factors protect replication fork progression and therefore DNA integrity.
Research published in the current issue of Cell — led by investigators at the Friedrich Miescher Institute for Biomedical Research in Basel, Switzerland — demonstrates that "microRNAs in retinal neurons decay much faster than microRNAs in non-neuronal cells." Increased microRNA turnover, the authors write, is characteristic of microRNAS in hippocampal and cortical neurons, as well as neurons differentiated from embryonic stem cells in vitro. The team concludes that neuronal microRNA metabolism is higher than that seen in most other cell types, and links to neuronal activity.
Investigators at Harvard Medical School, the Dana-Farber Cancer Institute, and the University of Montreal report that DCC — a transmembrane receptor — regulates translation and associates with protein synthesis machinery in Cell this week. "DCC colocalizes in particles with translation machinery and newly synthesized protein" in neuronal axons and dendrites, the authors write, adding that "the functional and physical association of a cell surface receptor with the translation machinery leads to a generalizable model for localization and extracellular regulation of protein synthesis."
A Westmead Institute for Cancer Research in New South Wales, Australia-led team reports in Cell this week that "IGFBP7 is not required for B-RAF-induced melanocyte senescence" — a finding which contrasts those of previous reports. The team writes that unlike other studies, theirs does not show that B-RAF signaling induces IGFBP7 expression, nor the expression of its targets, in human melanocytes or fibroblasts. "We also found no correlation between B-RAF mutational status and IGFBP7 protein expression levels in 22 melanoma cell lines, 90 melanomas, and 46 benign nevi," the authors write.