Department of Anatomy, Cell and Developmental Biology, Eötvös Loránd University (ELTE), Pázmány Péter sétány 1/C, Budapest, 1117, Hungary.
Momentum Vesicle Trafficking Research Group, Hungarian Academy of Sciences-Eötvös Loránd University, Budapest, Hungary.
Sci Rep. 2024 May 2;14(1):10146. doi: 10.1038/s41598-024-59775-0.
The closely related endolysosomal tethering complexes HOPS and CORVET play pivotal roles in the homo- and heterotypic fusion of early and late endosomes, respectively, and HOPS also mediates the fusion of lysosomes with incoming vesicles including late endosomes and autophagosomes. These heterohexameric complexes share their four core subunits that assemble with additional two, complex-specific subunits. These features and the similar structure of the complexes could allow the formation of hybrid complexes, and the complex specific subunits may compete for binding to the core. Indeed, our biochemical analyses revealed the overlap of binding sites for HOPS-specific VPS41 and CORVET-specific VPS8 on the shared core subunit VPS18. We found that the overexpression of CORVET-specific VPS8 or Tgfbrap1 decreased the amount of core proteins VPS11 and VPS18 that are assembled with HOPS-specific subunits VPS41 or VPS39, indicating reduced amount of assembled HOPS. In line with this, we observed the elevation of both lipidated, autophagosome-associated LC3 protein and the autophagic cargo p62 in these cells, suggesting impaired autophagosome-lysosome fusion. In contrast, overexpression of HOPS-specific VPS39 or VPS41 did not affect the level of assembled CORVET or autophagy. VPS8 or Tgfbrap1 overexpression also induced Cathepsin D accumulation, suggesting that HOPS-dependent biosynthetic delivery of lysosomal hydrolases is perturbed, too. These indicate that CORVET-specific subunit levels fine-tune HOPS assembly and activity in vivo.
紧密相关的内溶酶体连接复合物 HOPS 和 CORVET 分别在早期和晚期内体的同质和异质融合中发挥关键作用,HOPS 还介导包含晚期内体和自噬体的进入囊泡与溶酶体的融合。这些异六聚体复合物共享组装的四个核心亚基,以及两个特定于复合物的亚基。这些特征和复合物的相似结构可能允许形成混合复合物,并且特定于复合物的亚基可能竞争与核心结合。事实上,我们的生化分析揭示了 HOPS 特异性 VPS41 和 CORVET 特异性 VPS8 对共享核心亚基 VPS18 的结合位点的重叠。我们发现 CORVET 特异性 VPS8 或 Tgfbrap1 的过表达减少了与 HOPS 特异性亚基 VPS41 或 VPS39 组装的核心蛋白 VPS11 和 VPS18 的量,表明组装的 HOPS 量减少。与此一致,我们观察到这些细胞中脂质化的、与自噬体相关的 LC3 蛋白和自噬 cargo p62 的增加,表明自噬体 - 溶酶体融合受损。相比之下,HOPS 特异性 VPS39 或 VPS41 的过表达不会影响组装的 CORVET 或自噬的水平。VPS8 或 Tgfbrap1 的过表达也诱导组织蛋白酶 D 的积累,表明 HOPS 依赖性溶酶体水解酶的生物合成递呈也受到干扰。这些表明 CORVET 特异性亚基水平在体内精细调节 HOPS 的组装和活性。