Mutants in trs120 disrupt traffic from the early endosome to the late Golgi.
Mutants in trs120 disrupt traffic from the early endosome to the late Golgi.
复制标题
DOI：
10.1083/jcb.200505145
复制
发表时间：
2005-12-05
影响因子：
7.8
通讯作者：
Ferro-Novick, Susan
中科院分区：
文献类型：
--
作者：
Cai, Huaqing;Zhang, Yueyi;Pypaert, Marc;Walker, Lee;Ferro-Novick, Susan
转运蛋白颗粒（TRAPP）是一种介导膜运输的大型复合物，有两种形式（TRAPPI和-II）。这两种复合物共有7个亚基，而Trs130p、-120p和-65p这3个亚基是trappi特异性的。先前的研究表明，trappi特异性基因trs130的突变阻断了通过或来自高尔基体的交通。令人惊讶的是，我们报道trs120的突变不会阻断一般分泌。相反，trs120突变体积累了类似于伯克利体的异常膜结构，并破坏了通过早期核内体循环的蛋白质的运输。再生缺陷突变体也表现出外壳蛋白I （COPI）亚基定位缺陷，这意味着Trs120p可能参与早期内体途径中COPI依赖的运输步骤。此外，我们证明Trs120p与晚期高尔基标记Sec7p在很大程度上是共定位的。我们的研究结果表明Trs120p是早期核内体到晚期高尔基体的囊泡运输所必需的。
Transport protein particle (TRAPP), a large complex that mediates membrane traffic, is found in two forms (TRAPPI and -II). Both complexes share seven subunits, whereas three subunits (Trs130p, -120p, and -65p) are specific to TRAPPII. Previous studies have shown that mutations in the TRAPPII-specific gene trs130 block traffic through or from the Golgi. Surprisingly, we report that mutations in trs120 do not block general secretion. Instead, trs120 mutants accumulate aberrant membrane structures that resemble Berkeley bodies and disrupt the traffic of proteins that recycle through the early endosome. Mutants defective in recycling also display a defect in the localization of coat protein I (COPI) subunits, implying that Trs120p may participate in a COPI-dependent trafficking step on the early endosomal pathway. Furthermore, we demonstrate that Trs120p largely colocalizes with the late Golgi marker Sec7p. Our findings imply that Trs120p is required for vesicle traffic from the early endosome to the late Golgi.