Neutrophils, the primary foot soldiers of the immune system, swarm to sites of infection and inflammation by following breadcrumb pathways made up of signaling molecules. But the human body is a complex place, and neutrophils are often simultaneously bombarded with multiple signals, some of which are more important than others. For example, signals of infection or tissue damage require more urgent attention than signals produced by other immune cells.
Cancer often starts with the reshuffling of DNA—akin to scrambling the pages of a dictionary. Exactly how this happens has long been a mystery. But researchers in the UC Davis College of Biological Sciences have now arrived at one promising explanation.
The problem seems to happen at a critical moment: when the cell is fixing a broken string of DNA. This repair process, called homologous recombination, can go awry, says Wolf-Dietrich Heyer, a Distinguished Professor and chair in the Department of Microbiology and Molecular Genetics.
Priya Shah, who holds appointments in the Departments of Microbiology and Molecular Genetics, and the Department of Chemical Engineering, is deciphering the behavior of the Zika virus on animal cells to delve into the possibilities for mitigating the sickness in humans.
"My lab is really interested in how viruses hijack cells and turn them into little, tiny viral factories," said Shah.
A new study shows exactly how the gene BRCA2, linked to susceptibility to breast and ovarian cancer, functions to repair damaged DNA. By studying BRCA2 at the level of single molecules, researchers at the University of California, Davis, have generated new insights into the mechanisms of DNA repair and the origins of cancer. The work was published the week of March 27 in the Proceedings of the National Academy of Sciences.
