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© The Rockefeller University Press, 0021-9525/1999/10/163/ $5.00
The Journal of Cell Biology, Volume 147, Number 1, October 4, 1999 163-174


Original Article

Cell Wall Stress Depolarizes Cell Growth Via Hyperactivation of RHO1

Pierre-Alain Delleya and Michael N. Halla
a Department of Biochemistry, Biozentrum, University of Basel, CH-4056 Basel, Switzerland

Correspondence to: Michael N. Hall, Department of Biochemistry, Biozentrum, University of Basel, Klingelbergstrasse 70, CH-4056 Basel, Switzerland. Tel:41-61-267-2162 Fax:41-61-267-2149 E-mail:hall{at}ubaclu.unibas.ch.

Cells sense and physiologically respond to environmental stress via signaling pathways. Saccharomyces cerevisiae cells respond to cell wall stress by transiently depolarizing the actin cytoskeleton. We report that cell wall stress also induces a transient depolarized distribution of the cell wall biosynthetic enzyme glucan synthase FKS1 and its regulatory subunit RHO1, possibly as a mechanism to repair general cell wall damage. The redistribution of FKS1 is dependent on the actin cytoskeleton. Depolarization of the actin cytoskeleton and FKS1 is mediated by the plasma membrane protein WSC1, the RHO1 GTPase switch, PKC1, and a yet-to-be defined PKC1 effector branch. WSC1 behaves like a signal transducer or a stress-specific actin landmark that both controls and responds to the actin cytoskeleton, similar to the bidirectional signaling between integrin receptors and the actin cytoskeleton in mammalian cells. The PKC1-activated mitogen-activated protein kinase cascade is not required for depolarization, but rather for repolarization of the actin cytoskeleton and FKS1. Thus, activated RHO1 can mediate both polarized and depolarized cell growth via the same effector, PKC1, suggesting that RHO1 may function as a rheostat rather than as a simple on-off switch.

Key Words: actin cytoskeleton, yeast, PKC1, integrins, WSC1


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