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体内依赖Drs2p形成的胞吐网格蛋白包被囊泡

Drs2p-dependent formation of exocytic clathrin-coated vesicles in vivo.

作者信息

Gall Walter E, Geething Nathan C, Hua Zhaolin, Ingram Michael F, Liu Ke, Chen Sophie I, Graham Todd R

机构信息

Department of Biological Sciences, Vanderbilt University, Nashville, TN 37235-1634, USA.

出版信息

Curr Biol. 2002 Sep 17;12(18):1623-7. doi: 10.1016/s0960-9822(02)01148-x.

Abstract

The small GTP binding protein ARF has been implicated in budding clathrin-coated vesicles (CCVs) from Golgi and endosomal membranes. An arf1 synthetic lethal screen identified DRS2/SWA3 along with a clathrin heavy-chain conditional allele (chc1-5/swa5-1) and SWA2, encoding the yeast auxilin-like protein involved in uncoating CCVs. Drs2p/Swa3p is a P-type ATPase and a potential aminophospholipid translocase that localizes to the trans-Golgi network (TGN) in yeast. Genetic and phenotypic analyses of drs2Delta mutants suggested that Drs2p was required for clathrin function. To address a potential role for Drs2p in CCV formation from the TGN in vivo, we have performed epistasis analyses between drs2 and mutations that cause accumulation of distinct populations of post-Golgi vesicles. We find that Drs2p is required to form a specific class of secretory vesicles that accumulate when the actin cytoskeleton is disrupted. Accumulation of these vesicles also requires clathrin and is perturbed by mutation of AP-1, but not AP-2, AP-3, or GGA adaptins. Most of the accumulated vesicles are uncoated; however, clathrin coats can be partially stabilized on these vesicles by deletion of SWA2. These data provide the first in vivo evidence for an integral membrane protein requirement in forming CCVs.

摘要

小GTP结合蛋白ARF参与从高尔基体膜和内体膜上出芽形成网格蛋白包被小泡(CCV)的过程。一项arf1合成致死筛选鉴定出DRS2/SWA3,以及一个网格蛋白重链条件等位基因(chc1-5/swa5-1)和SWA2,SWA2编码参与CCV脱包被的酵母辅助蛋白样蛋白。Drs2p/Swa3p是一种P型ATP酶,也是一种潜在的氨基磷脂转位酶,定位于酵母的反式高尔基体网络(TGN)。drs2Δ突变体的遗传和表型分析表明,Drs2p是网格蛋白功能所必需的。为了研究Drs2p在体内从TGN形成CCV过程中的潜在作用,我们对drs2与导致不同高尔基体后小泡群体积累的突变进行了上位性分析。我们发现,Drs2p是形成一类特定分泌小泡所必需的,当肌动蛋白细胞骨架被破坏时这类小泡会积累。这些小泡的积累也需要网格蛋白,并且会受到AP-1突变的干扰,但不受AP-2、AP-3或GGA衔接蛋白突变的影响。大多数积累的小泡是未包被的;然而,通过缺失SWA2,网格蛋白包被可以在这些小泡上部分稳定。这些数据首次提供了体内证据,证明形成CCV需要一种整合膜蛋白。

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