IDI-WIP Seminar Series: Isabella Prislusky

Synpopsis:

Plasma membrane repair is a fundamental homeostatic process that protects eukaryotic cells from the extracellular environment. The plasma membrane is damaged during physiological body functions (e.g., physical exercise and heart beating) as well as during disease states (e.g., bacterial infections, inflammation, cancer, and neurodegenerative diseases) and dysregulation in repair can lead to chronic or acute pathologies. During infection, Listeria monocytogenes uses its virulence factor listeriolysin O (LLO) to perforate the plasma membrane. We have reported a new function for the septin cytoskeletal proteins in the repair of cells perforated by pore-forming toxins or mechanical disruption. Upon plasma membrane injury, the septin cytoskeleton is extensively redistributed to form sub membranous domains arranged as knob and loop structures containing F-actin, myosin IIA, S100A11, and ANXA2. Collectively, our data supports a novel model in which the septin cytoskeleton acts as a scaffold to promote the formation of plasma membrane repair domains containing contractile F-actin, ANXA2 and S100A11.