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Research summary:Wound healing impairment represents a major public health problem that is increasing due to an aging population and a sharp rise in the incidence of diabetes. Thus, understanding the molecular mechanisms of cell and tissue wound repair is both of biological interest and significant clinical relevance. Our long-term goal is to understand the molecular and cellular mechanisms of wound healing, using a combination of genetics, laser and mechanical wounding, and live imaging approaches. Our previous studies have established the adult C. elegans skin as a tractable genetic model system to dissect mechanisms of wound healing. We found an ancient and evolutionarily conserved role for Ca2+ as an early wound response signal in wound repair. Ca2+ signaling promotes actin cytoskeletal reorganization at wound sites by modulating the activity of Rho small GTPases. We further found that epidermal wounding also triggers rapid and local production of mitochondrial superoxide, which promote wound closure. Our lab will focus on the dissection the logic of wound responses and explore the molecular and cellular mechanism of repair processes. The extensive biochemical knowledge of wound signaling will allow these discoveries to guide the design of therapies that may be relevant to chronic wound healing pathologies in the diabetic and aging population.