cdc42 regulates the exit of apical and basolateral proteins from the trans-Golgi network
cdc42 regulates the exit of apical and basolateral proteins from the trans-Golgi network
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DOI：
10.1093/emboj/20.9.2171
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发表时间：
2001-05-01
期刊：
影响因子：
11.4
通讯作者：
Rodriguez-Boulan, E
中科院分区：
文献类型：
--
作者：
Müsch, A;Cohen, D;Rodriguez-Boulan, E
众所周知，Rho-GTPases通过其对皮质肌动蛋白细胞骨架的调节作用来调节质膜上的囊泡融合和分裂事件。相反，它们对细胞内运输过程和肌动蛋白池的影响不太清楚。最近的研究表明，cdc 42协会与高尔基体在一个ARF依赖的方式，类似于外壳蛋白参与囊泡的形成和几个肌动蛋白结合蛋白。我们在这里报告，cdc 42的突变体抑制出口的基底外侧蛋白质的trans-Golgi网络（TGN），而刺激出口的顶端标记，在两个不同的运输试验。这种调节可能是由于肌动蛋白细胞骨架的调节，因为GTP酶缺陷的cdc 42耗尽了与外源荧光肌动蛋白快速交换的核周肌动蛋白池。
It is well established that Rho-GTPases regulate vesicle fusion and fission events at the plasma membrane through their modulatory role on the cortical actin cytoskeleton. In contrast, their effects on intracellular transport processes and actin pools are less clear. It was recently shown that cdc42 associates with the Golgi apparatus in an ARF-dependent manner, similarly to coat proteins involved in vesicle formation and to several actin-binding proteins. We report here that mutants of cdc42 inhibited the exit of basolateral proteins from the trans-Golgi network (TGN), while stimulating the exit of an apical marker, in two different transport assays. This regulation may result from modulation of the actin cytoskeleton, as GTPase-deficient cdc42 depleted a perinuclear actin pool that rapidly exchanges with exogenous fluorescent actin.