Gillian Stanfield, PhD, is an associate professor in the Department of Human Genetics at the University of Utah and an adjunct member of the Cell Response and Regulation Program at the Huntsman Cancer Institute.
Stanfield studies cell motility, a process critical for development and wound healing that must be tightly regulated to prevent birth defects, the spread of cancer cells, and other adverse effects. Using genetic screens, she is identifying molecular pathways that regulate the ability of cells to migrate. She has found that motility is regulated in part by the opposing activities of a protease and protease inhibitor, suggesting a direct signaling role for proteolysis activity in this and other cell types. She is currently investigating how cells interpret such signals and respond with morphological rearrangements that allow them to migrate. In another line of research, she is studying how migratory behaviors and environmental cues contribute to competition among cells to occupy a niche.
Stanfield received an AB degree from the University of Chicago and a PhD from the Massachusetts Institute of Technology. She did postdoctoral research at Stanford University before coming to the University of Utah.
Research Statement
The Stanfield Lab studies cell motility, a process critical for development and wound healing that must be tightly regulated to prevent birth defects, the spread of cancer cells, and other adverse effects. Using genetic screens, we are identifying molecular pathways that regulate the ability of cells to migrate. We have found that motility is regulated in part by the opposing activities of a protease and protease inhibitor, suggesting a signaling role for proteolysis activity in this and other cell types. We are currently investigating how cells interpret such signals and respond with morphological rearrangements that allow them to migrate. In another line of research, we are studying competition between cells to migrate into and occupy a target tissue ("niche"). We are using in vivo observations of migrating cells to understand cellular behaviors that allow cells to outcompete other cells. We are also studying extrinsic signals that affect competition. All our studies utilize the powerful genetic, cell biological, and imaging tools available in the nematode C. elegans, focusing on sperm cells as our model cell type; since nematode spermatozoa lack flagella and instead migrate by crawling, they are analogous to many migratory cell types beyond the reproductive system.
