Osmotically induced cell volume changes alter anterograde and retrograde transport, Golgi structure, and COPI dissociation
Osmotically induced cell volume changes alter anterograde and retrograde transport, Golgi structure, and COPI dissociation
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DOI：
10.1091/mbc.10.5.1445
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发表时间：
1999-05-01
影响因子：
3.3
通讯作者：
Linstedt, AD
中科院分区：
文献类型：
--
作者：
Lee, TH;Linstedt, AD
影响组成交通和影响细胞器结构的生理条件尚不清楚。我们报告称，渗透压诱导的细胞体积变化（已知在多种条件下发生）会迅速抑制哺乳动物细胞中的内质网（ER）至高尔基体的转运。内质网输出和内质网高尔基体中间室 (ERGIC) 至高尔基体的运输步骤均被阻断，但逆行运输活跃，并且它介导 ERGIC 和高尔基体塌陷到内质网中。在低渗条件下观察到广泛的管状结构和相对快速的高尔基体驻留重新分布，而在高渗条件下观察到相同标记物的较慢的重新分布，没有明显的管状结构。渗透应激反应与 COPI 功能的扰动相关，因为低渗和高渗条件都会减慢布雷菲德菌素 A 诱导的 β COP 从高尔基膜的解离。值得注意的是，高尔基体居民在低渗或高渗介质中持续孵育几个小时后重新出现。重新出现与新蛋白质合成无关，但需要 PKC，这是一种已知介导细胞体积恢复的活性。总而言之，这些结果表明细胞体积和组成性交通之间存在耦合，通过对顺行和逆行流的独立影响来影响细胞器结构，并且部分涉及 COPI 功能的调节。
Physiological conditions that impinge on constitutive traffic and affect organelle structure are not known. We report that osmotically induced cell volume changes, which are known to occur under a variety of conditions, rapidly inhibited endoplasmic reticulum (ER)-to-Golgi transport in mammalian cells. Both ER export and ER Golgi intermediate compartment (ERGIC)-to-Golgi trafficking steps were blocked, but retrograde transport was active, and it mediated ERGIC and Golgi collapse into the ER. Extensive tubulation and relatively rapid Golgi resident redistribution were observed under hypo-osmotic conditions, whereas a slower redistribution of the same markers, without apparent tubulation, was observed under hyperosmotic conditions. The osmotic stress response correlated with the perturbation of COPI function, because both hypo- and hyperosmotic conditions slowed brefeldin A-induced dissociation of beta COP from Golgi membranes. Remarkably, Golgi residents reemerged after several hours of sustained incubation in hypotonic or hypertonic medium. Reemergence was independent of new protein synthesis but required PKC, an activity known to mediate cell volume recovery. Taken together these results indicate the existence of a coupling between cell volume and constitutive traffic that impacts organelle structure through independent effects on anterograde and retrograde flow and that involves, in part, modulation of COPI function.