Rab and actomyosin-dependent fission of transport vesicles at the Golgi complex
Rab and actomyosin-dependent fission of transport vesicles at the Golgi complex
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DOI：
10.1038/ncb2067
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发表时间：
2010-07-01
影响因子：
21.3
通讯作者：
Echard, A.
中科院分区：
文献类型：
--
作者：
Miserey-Lenkei, S.;Chalancon, G.;Echard, A.
膜隔室之间的运输是真核细胞的特征，并且依赖于在被运输并与正确的受体隔室融合之前从供体膜出芽和分裂的运输载体。Rab GTP酶通过调节转运载体沿着细胞骨架轨道的运动以及对接和融合过程所需的系留因子的募集来确保运输步骤的特异性和方向性。在这里，我们表明，Rab6，高尔基体相关的Rab，形成一个复杂的肌球蛋白II，有助于其本地化的高尔基复合体，出乎意料的是，控制Rab6囊泡的裂变。Rab6或肌球蛋白II功能的抑制损害Rab6转运载体从高尔基体膜的分裂和从高尔基体的顺行和逆行货物的运输。这些作用与肌球蛋白II在这些过程中是Rab6的效应子一致。我们的研究结果提供的证据表明，肌动球蛋白系统所需的囊泡生物发生在高尔基体，并揭示了一个功能的Rab GTP酶囊泡分裂。
Trafficking between membrane compartments is a characteristic of eukaryotic cells and relies on transport carriers that bud and fission from a donor membrane, before being transported and fusing with the correct acceptor compartment. Rab GTPases ensure specificity and directionality of trafficking steps by regulating the movement of transport carriers along cytoskeletal tracks, and the recruitment of tethering factors required for the docking and fusion processes. Here we show that Rab6, a Golgi-associated Rab, forms a complex with myosin II, contributes to its localization at the Golgi complex and, unexpectedly, controls the fission of Rab6 vesicles. Inhibition of either Rab6 or myosin II function impairs both the fission of Rab6 transport carriers from Golgi membranes and the trafficking of anterograde and retrograde cargo from the Golgi. These effects are consistent with myosin II being an effector of Rab6 in these processes. Our results provide evidence that the actomyosin system is required in vesicle biogenesis at the Golgi, and uncover a function for Rab GTPases in vesicle fission.