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Control of Cell Movement by Actomyosin Contractility and Cytoplasmic Pressure

Wednesday, September 23, 2020

9:00 AM-10:30 AM

BIOMED Seminar

Control of Cell Movement by Actomyosin Contractility and Cytoplasmic Pressure

Ryan Petrie, PhD
Assistant Professor
Department of Biology
College of Arts and Sciences
Drexel University

Human fibroblasts can switch between lamellipodia-dependent and -independent migration mechanisms on 2D surfaces and in 3D matrices. RhoA GTPase activity governs the switch from low-pressure lamellipodia to high-pressure lobopodia in response to the physical structure of the 3D matrix. Inhibiting actomyosin contractility in these cells reduces intracellular pressure and reverts lobopodia to lamellipodial protrusions via an unknown mechanism.

To test the hypothesis that high pressure physically prevents lamellipodia formation, we manipulated pressure by activating RhoA or changing the osmolarity of the extracellular environment and imaged cell protrusions and dynamics. Our results suggest that actomyosin contractility and water influx are coordinated to increase intracellular pressure and RhoA signaling can inhibit lamellipodia formation via two distinct pathways in high-pressure cells.

Ryan Petrie, PhD, is an assistant professor in the Department of Biology in the College of Arts and Sciences at Drexel University. Ryan received a BS in biochemistry from the University of Victoria in 1997, an MS in immune cell signaling from the University of Calgary in 2002, and a PhD in cell biology from McGill University in 2008. Following a research fellowship at the National Institutes of Health (NIH), he opened his lab at Drexel in 2015. At NIH, Dr. Petrie used a combination of live cell imaging and biophysical measurements in single cells to discover a new pressure-based mechanism of cell movement. His lab in the Department of Biology continues to investigate how pressure governs cell dynamics.

Contact Information

Lin Han

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