Hicke L, Riezman H
Department of Biochemistry, Biozentrum, University of Basel, Switzerland.
Cell. 1996 Jan 26;84(2):277-87. doi: 10.1016/s0092-8674(00)80982-4.
Binding of alpha factor to Ste2p, a G protein-coupled plasma membrane receptor, activates a signal transduction pathway and stimulates endocytosis of the receptor-ligand complex. Ligand binding also induces ubiquitination of the Ste2p cytoplasmic tail. Protein ubiquitination is required for stimulated endocytosis of Ste2p, as internalization is 5- to 15-fold slower in ubc mutants that lack multiple ubiquitin-conjugating enzymes. In a C-terminal truncated form of Ste2p that is rapidly ubiquitinated and endocytosed in response to ligand binding, a single lysine to arginine substitution in its cytoplasmic tail eliminates both ubiquitination and internalization. Thus, ubiquitination of Ste2p itself is required for ligand-stimulated endocytosis. We propose that ubiquitination mediates degradation of receptor-ligand complexes, not via the proteasome, but by acting as a signal for endocytosis leading to subsequent degradation in the lysosome/vacuole.
α因子与G蛋白偶联的质膜受体Ste2p结合,激活信号转导途径并刺激受体 - 配体复合物的内吞作用。配体结合还诱导Ste2p细胞质尾巴的泛素化。蛋白质泛素化是Ste2p受刺激内吞作用所必需的,因为在缺乏多种泛素结合酶的ubc突变体中,内化速度要慢5至15倍。在一种C末端截短形式的Ste2p中,其在配体结合后迅速泛素化并被内吞,其细胞质尾巴中的单个赖氨酸到精氨酸取代消除了泛素化和内化。因此,Ste2p自身的泛素化是配体刺激内吞作用所必需的。我们提出,泛素化介导受体 - 配体复合物的降解,不是通过蛋白酶体,而是作为内吞作用的信号,导致随后在溶酶体/液泡中降解。