A Dynamic Duo Promote Wound Healing: Genetics and Chemical Inhibitors

Friday, October 28, 2011
Room A2/A7 (San Jose Convention Center)
Michelle Juarez, PhD , University of California, San Diego, La Jolla, CA
William McGinnis, PhD , Department of Biology, University of California San Diego, La Jolla, CA
A break in the epidermal barrier elicits a wide range of responses, including clot formation, reepithelialization, cell proliferation, inflammation, and barrier replacement.  As a first line of defense, an organism must not only initiate a wound response but also coordinate the wound signals around the site of injury.  Failure to properly control the wound response can alter survival after injury.  To better understand what signals promote wound healing we are testing chemical compounds as potential activators of an epidermal wound response.  The Drosophila embryo provides an excellent system to both injure and detect activation of wound response with in vivo fluorescent reporters.  Using a micro-pipette we simultaneously wound and deliver the chemical compounds to the embryo.  Results identify that cholesterol depletion, oxidation, and serine protease treatments can activate a wound response throughout the epidermis of the Drosophila embryo.  Combining the chemical compound tests with results from a genetic screen provides insights into the mechanisms that control the epidermal wound response.  Using Drosophila to determine factors that coordinate the activation of the epidermal wound response and the signaling that occurs between cells at the site of injury brings new understanding to a complex problem faced by all multi-cellular organisms.