Skip to Content
Michael Galko

Michael Galko

Regular Member


[email protected]
BSRB S11.8116B

The University of Texas MD Anderson Cancer Center
Department of Genetics

Multicellular organisms have evolved a variety of tissue repair responses to cope with tissue damage. Some of these responses (wound closure) are aimed at restoring structure and function to the damaged tissue(s) while others (nociceptive sensitization) are aimed at protecting the organism from further injury. My laboratory is interested in identifying the elusive signals that initiate and terminate different aspects of the organismal tissue repair response, as well as the genes that are required to execute each specific response.  Ultimately, we wish to understand in molecular detail how the activities of diverse damage-responsive cell types are coordinated in space and time to give a functional tissue repair program. To pursue these interests we have developed a variety of tissue repair/response assays in the highly genetically tractable model organism, Drosophila melanogaster and are focusing our efforts on two critical responses: epidermal wound closure and nociceptive sensitization (lowering of the threshold for sensing painful stimuli following injury).  Given that tissue repair responses are an ancient survival mechanism of multicellular animals, we expect that the functional importance of many of these genes we identify will be conserved between flies and vertebrates.  To date, this suspicion has been borne out:  My lab has identified two conserved pathways involved in epidermal wound closure (Jun N-terminal Kinase signaling and VEGF signaling) and nociceptive sensitization (Tumor Necrosis Factor and Hedgehog).  A major goal of our work is to turn Drosophila into a powerful translational research tool that discovers genes with high potential for translation to clinical application.


MDACC Faculty

Galko Lab

Education & Training

PhD, University of California, San Francisco, 1999

Research Info

Drosophila genetics; molecular genetics of tissue repair; cell migration; cell signaling and signal transduction; pain sensitization

Research Opportunities


Faculty Development