Pineda-Molina Estela, Belrhali Hassan, Piefer Andrew J, Akula Indira, Bates Paul, Weissenhorn Winfried
European Molecular Biology Laboratory (EMBL), 6 rue Jules Horowitz, 38042 Grenoble, France.
Traffic. 2006 Aug;7(8):1007-16. doi: 10.1111/j.1600-0854.2006.00440.x. Epub 2006 Jun 2.
The endosomal sorting complex I required for transport (ESCRT-I) is composed of the three subunits Vps23/Tsg101, Vps28 and Vps37. ESCRT-I is recruited to cellular membranes during multivesicular endosome biogenesis and by enveloped viruses such as HIV-1 to mediate budding from the cell. Here, we describe the crystal structure of a conserved C-terminal domain from Sacharomyces cerevisiae Vps28 (Vps28-CTD) at 3.05 A resolution which folds independently into a four-helical bundle structure. Co-expression experiments of Vps28-CTD, Vps23 and Vps37 suggest that Vps28-CTD does not directly participate in ESCRT-I assembly and may thus act as an adaptor module for downstream interaction partners. We show through mutagenesis studies that Vps28-CTD employs its strictly conserved surface in the interaction with the ESCRT-III factor Vps20. Furthermore, we present evidence that Vps28-CTD is sufficient to rescue an equine infectious anaemia virus (EIAV) Gag late domain deletion. Vps28-CTD mutations abolishing Vps20 interaction in vitro also prevent the rescue of the EIAV Gag late domain mutant consistent with a potential direct Vps28-ESCRT-III Vps20 recruitment. Therefore, the physiological relevant EIAV Gag-Alix interaction can be functionally replaced by a Gag-Vps28-CTD fusion. Because both Alix and Vps28-CTD can directly recruit ESCRT-III proteins, ESCRT-III assembly coupled to Vps4 action may therefore constitute the minimal budding machinery for EIAV release.
转运所需的内体分选复合体I(ESCRT-I)由Vps23/Tsg101、Vps28和Vps37这三个亚基组成。在多泡内体生物发生过程中以及被诸如HIV-1等包膜病毒招募时,ESCRT-I会被募集到细胞膜上,以介导从细胞中出芽。在此,我们描述了酿酒酵母Vps28的保守C末端结构域(Vps28-CTD)的晶体结构,分辨率为3.05埃,其独立折叠成四螺旋束结构。Vps28-CTD、Vps23和Vps37的共表达实验表明,Vps28-CTD不直接参与ESCRT-I的组装,因此可能作为下游相互作用伙伴的衔接模块。我们通过诱变研究表明,Vps28-CTD在与ESCRT-III因子Vps20的相互作用中利用其严格保守的表面。此外,我们提供证据表明,Vps28-CTD足以挽救马传染性贫血病毒(EIAV)Gag晚期结构域缺失。在体外消除Vps20相互作用的Vps28-CTD突变也阻止了EIAV Gag晚期结构域突变体的挽救,这与潜在的直接Vps28-ESCRT-III Vps20招募一致。因此,生理相关的EIAV Gag-Alix相互作用可以在功能上被Gag-Vps28-CTD融合所取代。由于Alix和Vps28-CTD都可以直接招募ESCRT-III蛋白,因此与Vps4作用偶联的ESCRT-III组装可能构成EIAV释放的最小出芽机制。