Division of Infectious Diseases, Department of Medicine, Massachusetts General Hospital, Cambridge, Massachusetts, USA.
J Bacteriol. 2014 Jan;196(2):367-77. doi: 10.1128/JB.01095-13. Epub 2013 Nov 1.
In bacteria, a subset of membrane proteins insert into the membrane via the Sec apparatus with the assistance of the widely conserved essential membrane protein insertase YidC. After threading into the SecYEG translocon, transmembrane segments of nascent proteins are thought to exit the translocon via a lateral gate in SecY, where YidC facilitates their transfer into the lipid bilayer. Interactions between YidC and components of the Sec apparatus are critical to its function. The first periplasmic loop of YidC interacts directly with SecF. We sought to identify the regions or residues of YidC that interact with SecY or with additional components of the Sec apparatus other than SecDF. Using a synthetic lethal screen, we identified residues of YidC that, when mutated, led to dependence on SecDF for viability. Each residue identified is highly conserved among YidC homologs; most lie within transmembrane domains. Overexpression of SecY in the presence of two YidC mutants partially rescued viability in the absence of SecDF, suggesting that the corresponding wild-type YidC residues (G355 and M471) participate in interactions, direct or indirect, with SecY. Staphylococcus aureus YidC complemented depletion of YidC, but not of SecDF, in Escherichia coli. G355 of E. coli YidC is invariant in S. aureus YidC, suggesting that this highly conserved glycine serves a conserved function in interactions with SecY. This study demonstrates that transmembrane residues are critical in YidC interactions with the Sec apparatus and provides guidance on YidC residues of interest for future structure-function analyses.
在细菌中,有一组膜蛋白通过 Sec 装置插入膜中,在广泛保守的必需膜蛋白插入酶 YidC 的协助下。在穿入 SecYEG 转运体后,新生蛋白质的跨膜片段被认为通过 SecY 中的侧门离开转运体,YidC 促进它们转移到脂质双层中。YidC 与 Sec 装置组件之间的相互作用对其功能至关重要。YidC 的第一个周质环直接与 SecF 相互作用。我们试图确定与 SecY 或 Sec 装置的其他组件(除了 SecDF)相互作用的 YidC 区域或残基。使用合成致死筛选,我们确定了 YidC 的残基,当这些残基发生突变时,会导致对 SecDF 的生存依赖。鉴定出的每个残基在 YidC 同源物中高度保守;大多数位于跨膜结构域内。在存在两种 YidC 突变体的情况下过表达 SecY 部分挽救了 SecDF 缺失时的生存能力,这表明相应的野生型 YidC 残基(G355 和 M471)参与了直接或间接与 SecY 的相互作用。金黄色葡萄球菌 YidC 可补充大肠杆菌中 YidC 的缺失,但不能补充 SecDF 的缺失。大肠杆菌 YidC 的 G355 在金黄色葡萄球菌 YidC 中是不变的,这表明这个高度保守的甘氨酸在与 SecY 的相互作用中具有保守的功能。本研究表明,跨膜残基在 YidC 与 Sec 装置的相互作用中至关重要,并为未来的结构功能分析提供了有关 YidC 感兴趣残基的指导。