Stress-mediated actin phosphorylation in endocytosis and age regulation
As humans age, our tissues and organs gradually deteriorate. Aging compromises the integrity of a tissue’s surrounding barrier, which leads to increased leakiness and dysfunction of the respective organs. This theory has been termed the “barrier dysfunction of aging.”
Using the intestine of the nematode C. elegans, Dr. Douglas and his team have uncovered a novel molecular mechanism involving stress-mediated actin phosphorylation, or addition of phosphate. Actin—a protein in muscle cells that allows the cells to move and function—plays a significant role in cellular transport, stress response, and human disease.
Dr. Douglas hypothesizes that actin phosphorylation drives tissue “leakiness,” and therefore accelerates the aging process. He and his team are working to better understand how it does so and what effect it has on the aging body. This knowledge would lead to a better understanding of tissue homeostasis in human physiology.