Diana Bautista

Diana M. Bautista is an American neuroscientist known for her work on the molecular mechanisms underlying itch, touch and pain. She is an associate professor of cell and developmental biology and is affiliated with the division of neurobiology at University of California, Berkeley.

Bautista was raised in Chicago and was the first member of her family to graduate high school. While taking a break from pursuing a fine arts degree, she worked for an environmental group in Chicago, which sparked her interest in the intersection of chemistry, the environment and human disease. This lead her to the University of Oregon to study environmental science. While working in the laboratory of Peter O'Day, she became interested in cell signaling and the nervous system. Dr. O'Day encouraged her apply for graduate school where she eventually chose to join the laboratory of Richard Lewis at Stanford University. For her graduate studies, Dr. Bautista used electrophysiology and calcium imaging to characterize how plasma-membrane calcium-ATPase (PMCA) and Ca(2+) release-activated Ca(2+) (CRAC) channels regulate calcium levels in T-cells.

As a post-doctoral fellow in David Julius's lab, she characterized the response profiles of TRPA1 and TRPM8 and the molecular target of Szechuan peppers. Previously, Dr. Bautista helped show that allyl isothiocyanate, a pungent chemical found in wasabi and other mustard plants, potently activates TRPA1. In a subsequent study, she demonstrated that compounds found in garlic plants, allicin and DADs, also activate TRPA1. Interestingly, both allicin, DADs and allyl isothiocyanate share structurally similar motifs, suggesting that Allium and Brassica plants independently derived chemical mechanisms to activate TRPA1 to deter potential predators. TRPA1 is also targeted by environmental irritants like acrolein, which is found in tear gas and vehicle exhaust. Using TRPA1-deficient mice, she showed that TRPA1 is activated by acrolein, allicin and allyl isothiocyanate, which in turn depolarizes nociceptors and elicits inflammatory pain. Dr. Bautista also developed TRPM8-deficient mice to demonstrate, using electrophysiology and behavioral studies, that TRPM8 is the target of cold and menthol stimuli.

In 2008, Bautista started her own lab at University of California, Berkeley and is a Rita Allen Scholar.