Cell wall stress depolarizes cell growth via hyperactivation of RHO1.
Cell wall stress depolarizes cell growth via hyperactivation of RHO1.
复制标题
DOI：
10.1083/jcb.147.1.163
复制
发表时间：
1999-10-04
影响因子：
7.8
通讯作者：
Hall, M N
中科院分区：
文献类型：
--
作者：
Delley, P A;Hall, M N
细胞通过信号通路感知环境压力并作出生理反应。酿酒酵母细胞通过肌动蛋白细胞骨架的瞬时去极化来响应细胞壁压力。我们报道细胞壁应激还诱导细胞壁生物合成酶葡聚糖合成酶FKS1及其调控亚基RHO1的短暂去极化分布，可能作为修复一般细胞壁损伤的机制。FKS1的再分配依赖于肌动蛋白细胞骨架。肌动蛋白骨架和FKS1的去极化是由质膜蛋白WSC1、RHO1 GTPase开关、PKC1和一个尚未定义的PKC1效应分支介导的。WSC1的行为类似于信号换能器或应激特异性肌动蛋白地标，控制并响应肌动蛋白细胞骨架，类似于哺乳动物细胞中整合素受体和肌动蛋白细胞骨架之间的双向信号传导。pkc1激活的丝裂原激活的蛋白激酶级联不是去极化所必需的，而是肌动蛋白骨架和FKS1的再极化所必需的。因此，激活的RHO1可以通过相同的效应物PKC1介导极化和去极化细胞的生长，这表明RHO1可能是一个变阻器，而不是一个简单的开关。
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.