Rubio-Texeira Marta, Kaiser Chris A
Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Mol Biol Cell. 2006 Jul;17(7):3031-50. doi: 10.1091/mbc.e05-07-0669. Epub 2006 Apr 26.
Intracellular sorting of the general amino acid permease (Gap1p) in Saccharomyces cerevisiae depends on availability of amino acids such that at low amino acid concentrations Gap1p is sorted to the plasma membrane, whereas at high concentrations Gap1p is sorted to the vacuole. In a genome-wide screen for mutations that affect Gap1p sorting we identified deletions in a subset of components of the ESCRT (endosomal sorting complex required for transport) complex, which is required for formation of the multivesicular endosome (MVE). Gap1p-GFP is delivered to the vacuolar interior by the MVE pathway in wild-type cells, but when formation of the MVE is blocked by mutation, Gap1p-GFP efficiently cycles from this compartment to the plasma membrane, resulting in unusually high permease activity at the cell surface. Importantly, cycling of Gap1p-GFP to the plasma membrane is blocked by high amino acid concentrations, defining recycling from the endosome as a major step in Gap1p trafficking under physiological control. Mutations in LST4 and LST7 genes, previously identified for their role in Gap1p sorting, similarly block MVE to plasma membrane trafficking of Gap1p. However, mutations in other recycling complexes such as the retromer had no significant effect on the intracellular sorting of Gap1p, suggesting that Gap1p follows a genetically distinct pathway for recycling. We previously found that Gap1p sorting from the Golgi to the endosome requires ubiquitination of Gap1p by an Rsp5p ubiquitin ligase complex, but amino acid abundance does not appear to significantly alter the accumulation of polyubiquitinated Gap1p. Thus the role of ubiquitination appears to be a signal for delivery of Gap1p to the MVE, whereas amino acid abundance appears to control the cycling of Gap1p from the MVE to the plasma membrane.
酿酒酵母中通用氨基酸通透酶(Gap1p)的细胞内分选取决于氨基酸的可用性,即低氨基酸浓度时Gap1p被分选到质膜,而高浓度时Gap1p被分选到液泡。在全基因组筛选影响Gap1p分选的突变时,我们鉴定出了内体转运所需分选复合体(ESCRT,endosomal sorting complex required for transport)的一部分组分中的缺失,该复合体是多泡内体(MVE)形成所必需的。在野生型细胞中,Gap1p-GFP通过MVE途径被递送到液泡内部,但当MVE的形成因突变而受阻时,Gap1p-GFP有效地从该区室循环到质膜,导致细胞表面的通透酶活性异常高。重要的是,高氨基酸浓度会阻断Gap1p-GFP循环到质膜,这将内体的循环定义为生理控制下Gap1p运输的一个主要步骤。先前已鉴定出在Gap1p分选过程中起作用的LST4和LST7基因中的突变,同样会阻断Gap1p从MVE到质膜的运输。然而,其他回收复合体(如逆转录酶复合体)中的突变对Gap1p的细胞内分选没有显著影响,这表明Gap1p遵循一条遗传上不同的回收途径。我们之前发现,Gap1p从高尔基体到内体的分选需要Rsp5p泛素连接酶复合体对Gap1p进行泛素化,但氨基酸丰度似乎不会显著改变多泛素化Gap1p的积累。因此,泛素化的作用似乎是将Gap1p递送到MVE的信号,而氨基酸丰度似乎控制着Gap1p从MVE到质膜的循环。