Cell wall stress depolarizes cell growth via hyperactivation of RHO1

Cells sense and physiologically respond to environmental stress via signali ng pathways. Saccharomyces cerevisiae cells respond to cell wall stress by transiently depolarizing the actin cytoskeleton. We report that cell wall s tress also induces a transient depolarized distribution of the cell wall bi osynthetic enzyme glucan synthase FKS1 and its regulatory subunit RHO1, pos sibly as a mechanism to repair general cell wall damage. The redistribution of FKS1 is dependent on the actin cytoskeleton. Depolarization of the acti n cytoskeleton and FKS1 is mediated by the plasma membrane protein WSC1, th e RHO1 GTPase switch, PKC1, and a yet-to-be defined PKC1 effector branch. W SC1 behaves like a signal transducer or a stress-specific actin landmark th at both controls and responds to the actin cytoskeleton, similar to the bid irectional signaling between integrin receptors and the actin cytoskeleton in mammalian cells. The PKC1-activated mitogen-activated protein kinase cas cade is not required for depolarization, but rather for repolarization of t he actin cytoskeleton and FKS1. Thus, activated RHO1 can mediate both polar ized and depolarized cell growth via the same effector, PKC1, suggesting th at RHO1 may function as a rheostat rather than as a simple on-off switch.