Ca 2+ regulation of Myosin II and Myosin VI during rupture of the Shigella -containing vacuole
Résumé
Shigella , the causative agent of bacillary dysentery, invades epithelial cells to colonize the intestinal mucosa. Following invasion, Shigella is enclosed in a vacuole that needs to rupture for bacterial intra-cytosolic replication. We show here that rupture of the Shigella vacuole requires Ca 2+ influx leading to long lasting local Ca 2+ increases that regulate actin dynamics affecting the Shigella vacuole integrity. These Ca 2+ increases promote vacuolar rupture by activating myosin II associated with actin filaments in membrane ruffles distant from the vacuole, while tethering myosin VI at the actin coat-surrounded vacuole. Ca 2+ depletion and myosin II inhibition impair formation of the actin coat and vacuole rupture. Inhibition of myosin VI also delays rupture of vacuoles but lead to their tumbling. These findings highlight a role for Ca 2+ in coordinating actin–based forces and constraints during early rupture steps of bacterial vacuole, that pull on vacuolar membranes and tether them to the actin cortex via myosin II and VI, respectively, a process relevant to intracellular pathogen and endomembrane trafficking.
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