Auxilin facilitates membrane traffic in the early secretory pathway.
Auxilin facilitates membrane traffic in the early secretory pathway.
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DOI：
10.1091/mbc.e15-09-0631
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发表时间：
2016-01-01
影响因子：
3.3
通讯作者：
Ferro-Novick S
中科院分区：
文献类型：
--
作者：
Ding J;Segarra VA;Chen S;Cai H;Lemmon SK;Ferro-Novick S
在这项研究中，一种蛋白质组学的方法将J-结构域的伴侣蛋白生长素与细胞中的其他主要被膜复合体(COPII和COPI)连接起来。遗传学和生物化学研究支持这一观点，即在早期的分泌途径中，生长素促进小泡的运输。外壳蛋白复合体包含一个用于分类货物的内壳和一个帮助使膜变形以使囊泡成形的外壳。细胞中有三种主要类型的包膜囊泡：COPII、COPI和笼蛋白。COPII被膜复合体促进内质网(ER)的囊泡萌发，而COPI被膜复合体在高尔基体中起着类似的作用。笼状蛋白包裹的囊泡调节细胞表面以及反式高尔基体和内体之间的运输。虽然这些涂层复合体的组装和结构已经得到了广泛的研究，但对COPII和COPI涂层从膜上分解的了解较少。我们描述了一种蛋白质组学和遗传学方法，它将J-结构域的伴侣辅助素与COPII和COPI包衣复合体连接起来。与生长素在早期分泌途径中的功能作用一致，它与COPII和COPI外壳亚单位结合。此外，在缺少生长素的Sw2Δ突变细胞中，内质网高尔基体和高尔基体内的流量在15℃时延迟。在COPII囊泡的情况下，我们将这种延迟与囊泡融合中的缺陷联系起来。我们认为，在早期的分泌途径中，生长素作为一个伴侣和/或脱壳因子来运输小泡。
In this study, a proteomic approach links the J-domain chaperone auxilin, which uncoats clathrin-coated vesicles, to the other major coat complexes in the cell (COPII and COPI). Genetic and biochemical studies support the proposal that auxilin facilitates vesicle traffic in the early secretory pathway. Coat protein complexes contain an inner shell that sorts cargo and an outer shell that helps deform the membrane to give the vesicle its shape. There are three major types of coated vesicles in the cell: COPII, COPI, and clathrin. The COPII coat complex facilitates vesicle budding from the endoplasmic reticulum (ER), while the COPI coat complex performs an analogous function in the Golgi. Clathrin-coated vesicles mediate traffic from the cell surface and between the trans-Golgi and endosome. While the assembly and structure of these coat complexes has been extensively studied, the disassembly of COPII and COPI coats from membranes is less well understood. We describe a proteomic and genetic approach that connects the J-domain chaperone auxilin, which uncoats clathrin-coated vesicles, to COPII and COPI coat complexes. Consistent with a functional role for auxilin in the early secretory pathway, auxilin binds to COPII and COPI coat subunits. Furthermore, ER–Golgi and intra-Golgi traffic is delayed at 15°C in swa2Δ mutant cells, which lack auxilin. In the case of COPII vesicles, we link this delay to a defect in vesicle fusion. We propose that auxilin acts as a chaperone and/or uncoating factor for transport vesicles that act in the early secretory pathway.
影响因子：
7.8
作者：
Groesch, M E;Ruohola, H;Bacon, R;Rossi, G;Ferro-Novick, S
通讯作者：
Ferro-Novick, S