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Gillian Stanfield

Assistant Professor of Human Genetics

A.B. University of Chicago

Ph.D. Massachusetts Institute of Technology

Research

References

gillians@genetics.utah.edu

Gillian Stanfield's PubMed Literature Search

Research

Cell migrations are vital for shaping organs during development, for wound healing, and in many other contexts throughout the life of a multicellular animal. However, the ability to migrate must be held in check to prevent invasive cell movements, such as metastasis. Signals from the environment dictate whether to remain stationary or to become motile and specify the direction of migration. To understand these processes, we are studying a specific cell type, C. elegans sperm. Nematode sperm lack flagella and instead move by crawling. We are using these cells as a model for addressing a variety of questions about how cell motility is regulated.  For example:

Cellular differentiation: how do extracellular signals induce motility? Worm sperm are triggered to complete morphogenesis and become motile in response to specific signals. We have discovered that one such trigger involves an extracellular serine protease, TRY-5.  We are currently working to understand how TRY-5 activity is restricted to ensure that sperm activate only at appropriate places and times. In addition, we are investigating candidate targets for TRY-5 on sperm.  Interestingly, one potential target is SNF-10, a member of the SLC6 family of transporters, which play important roles in nervous system function and physiological processes in humans. Thus, our studies are providing insight into general mechanisms of cell signaling and homeostasis.

Cell competition: how do sperm cells compete for access to an egg? In C. elegans, male sperm must compete with a hermaphrodite's self sperm to fertilize her eggs. Interestingly, male sperm always wins. While it is clear that this effect is due to some intrinsic property of male sperm, the cellular behaviors required for this precedence effect are not well understood and the molecular mechanisms are completely mysterious. We are analyzing patterns of sperm cell movement that result in differential fertilization and characterizing a novel gene that we identified in a screen for mutants defective in male sperm precedence.  We hope to gain insight into conserved mechanisms that influence the ability of migratory cells to populate a niche.

 

Sperm migration in C. elegans. Male sperm were transferred to a hermaphrodite and are migrating bidirectionally around embryos through the uterus towards oocytes (not shown). (A) DIC image. (B) Fluorescence image. Red, Mitotracker-labeled sperm; yellow, seminal fluid components marking the transfer site (*). 

References