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利用半胱氨酸-二硫键交联监测内质网-高尔基体转运过程中的SNARE复合体组装

Cysteine-disulfide cross-linking to monitor SNARE complex assembly during endoplasmic reticulum-Golgi transport.

作者信息

Flanagan John J, Barlowe Charles

机构信息

Department of Biochemistry, Dartmouth Medical School, Hanover, NH 03755, USA.

出版信息

J Biol Chem. 2006 Jan 27;281(4):2281-8. doi: 10.1074/jbc.M511695200. Epub 2005 Nov 21.

Abstract

Assembly of cognate SNARE proteins into SNARE complexes is required for many intracellular membrane fusion reactions. However, the mechanisms that govern SNARE complex assembly and disassembly during fusion are not well understood. We have devised a new in vitro cross-linking assay to monitor SNARE complex assembly during fusion of endoplasmic reticulum (ER)-derived vesicles with Golgi-acceptor membranes. In Saccharomyces cerevisiae, anterograde ER-Golgi transport requires four SNARE proteins: Sec22p, Bos1p, Bet1p, and Sed5p. After tethering of ER-derived vesicles to Golgi-acceptor membranes, SNARE proteins are thought to assemble into a four-helix coiled-coil bundle analogous to the structurally characterized neuronal and endosomal SNARE complexes. Molecular modeling was used to generate a structure of the four-helix ER-Golgi SNARE complex. Based on this structure, cysteine residues were introduced into adjacent SNARE proteins such that disulfide bonds would form if assembled into a SNARE complex. Our initial studies focused on disulfide bond formation between the SNARE motifs of Bet1p and Sec22p. Expression of SNARE cysteine derivatives in the same strain produced a cross-linked heterodimer of Bet1p and Sec22p under oxidizing conditions. Moreover, this Bet1p-Sec22p heterodimer formed during in vitro transport reactions when ER-derived vesicles containing the Bet1p derivative fused with Golgi membranes containing the Sec22p derivative. Using this disulfide cross-linking assay, we show that inhibition of transport with anti-Sly1p antibodies blocked formation of the Bet1p-Sec22p heterodimer. In contrast, chelation of divalent cations did not inhibit formation of the Bet1p-Sec22p heterodimer during in vitro transport but potently inhibited Golgi-specific carbohydrate modification of glyco-pro-alpha factor. This data suggests that Ca(2+) is not directly required for membrane fusion between ER-derived vesicles and Golgi-acceptor membranes.

摘要

同源SNARE蛋白组装成SNARE复合体是许多细胞内膜融合反应所必需的。然而,在融合过程中控制SNARE复合体组装和解聚的机制尚未完全了解。我们设计了一种新的体外交联试验,以监测内质网(ER)衍生的囊泡与高尔基体受体膜融合过程中的SNARE复合体组装。在酿酒酵母中,顺行性内质网-高尔基体运输需要四种SNARE蛋白:Sec22p、Bos1p、Bet1p和Sed5p。在ER衍生的囊泡与高尔基体受体膜拴系后,SNARE蛋白被认为组装成一个四螺旋卷曲螺旋束,类似于结构上已表征的神经元和内体SNARE复合体。分子建模用于生成四螺旋内质网-高尔基体SNARE复合体的结构。基于此结构,将半胱氨酸残基引入相邻的SNARE蛋白中,使得如果组装成SNARE复合体就会形成二硫键。我们最初的研究集中在Bet1p和Sec22p的SNARE基序之间的二硫键形成。在同一菌株中表达SNARE半胱氨酸衍生物,在氧化条件下产生了Bet1p和Sec22p的交联异二聚体。此外,当含有Bet1p衍生物的ER衍生囊泡与含有Sec22p衍生物的高尔基体膜融合时,这种Bet1p-Sec22p异二聚体在体外运输反应过程中形成。使用这种二硫键交联试验,我们表明用抗Sly1p抗体抑制运输会阻止Bet1p-Sec22p异二聚体的形成。相反,二价阳离子的螯合在体外运输过程中不抑制Bet1p-Sec22p异二聚体的形成,但能有效抑制糖基化前α因子的高尔基体特异性糖基修饰。该数据表明,内质网衍生囊泡与高尔基体受体膜之间的膜融合并不直接需要Ca(2+)。

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