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Cell wall stress depolarizes cell growth via hyperactivation of RHO1.

Delley PA, Hall MN - J. Cell Biol. (1999)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry, Biozentrum, University of Basel, CH-4056 Basel, Switzerland.

ABSTRACT
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.

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Model for the regulation of actin cytoskeleton and FKS1 distribution upon cell wall stress (see Discussion for further details).
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Figure 6: Model for the regulation of actin cytoskeleton and FKS1 distribution upon cell wall stress (see Discussion for further details).

Mentions: We have shown that the actin cytoskeleton and the distribution of the cell wall synthesis enzyme glucan synthase (FKS1 and its regulatory subunit RHO1) are transiently depolarized in response to cell wall stress. In heat shocked or SDS-treated cells, actin patches and glucan synthase are redistributed from a polarized growth site (bud) to the periphery of the entire cell. This stress-induced depolarization of cell growth, possibly as a mechanism to repair general cell wall damage, is mediated by a putative signaling pathway consisting of the plasma membrane protein WSC1, the RHO1 exchange factor ROM2, RHO1, PKC1, and a yet-to-be identified PKC1 effector branch. The PKC1-activated MAP kinase pathway mediates repolarization of the actin cytoskeleton and FKS1. The de- and repolarization of FKS1 is dependent on the actin cytoskeleton. A model summarizing our results is shown in Fig. 6.


Cell wall stress depolarizes cell growth via hyperactivation of RHO1.

Delley PA, Hall MN - J. Cell Biol. (1999)

Model for the regulation of actin cytoskeleton and FKS1 distribution upon cell wall stress (see Discussion for further details).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2164985&req=5

Figure 6: Model for the regulation of actin cytoskeleton and FKS1 distribution upon cell wall stress (see Discussion for further details).
Mentions: We have shown that the actin cytoskeleton and the distribution of the cell wall synthesis enzyme glucan synthase (FKS1 and its regulatory subunit RHO1) are transiently depolarized in response to cell wall stress. In heat shocked or SDS-treated cells, actin patches and glucan synthase are redistributed from a polarized growth site (bud) to the periphery of the entire cell. This stress-induced depolarization of cell growth, possibly as a mechanism to repair general cell wall damage, is mediated by a putative signaling pathway consisting of the plasma membrane protein WSC1, the RHO1 exchange factor ROM2, RHO1, PKC1, and a yet-to-be identified PKC1 effector branch. The PKC1-activated MAP kinase pathway mediates repolarization of the actin cytoskeleton and FKS1. The de- and repolarization of FKS1 is dependent on the actin cytoskeleton. A model summarizing our results is shown in Fig. 6.

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry, Biozentrum, University of Basel, CH-4056 Basel, Switzerland.

ABSTRACT
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.

Show MeSH
Related in: MedlinePlus