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Ecm33 is a novel factor involved in efficient glucose uptake for nutrition‐responsive TORC 1 signaling in yeast
Author(s) -
Umekawa Midori,
Ujihara Masato,
Nakai Daiki,
Takematsu Hiromu,
Wakayama Mamoru
Publication year - 2017
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.12882
Subject(s) - extracellular , snf3 , signal transduction , intracellular , dephosphorylation , microbiology and biotechnology , saccharomyces cerevisiae , yeast , kinase , biochemistry , glucose uptake , autophagy , cell signaling , cell growth , biology , phosphorylation , chemistry , phosphatase , apoptosis , endocrinology , insulin
Glucose uptake is crucial for providing both an energy source and a signal that regulates cell proliferation. Therefore, it is important to clarify the mechanisms underlying glucose uptake and its transmission to intracellular signaling pathways. In this study, we searched for a novel regulatory factor involved in glucose‐induced signaling by using Saccharomyces cerevisiae as a eukaryotic model. Requirement of the extracellular protein Ecm33 in efficient glucose uptake and full activation of the nutrient‐responsive TOR kinase complex 1 ( TORC 1) signaling pathway is shown. Cells lacking Ecm33 elicit a series of starvation‐induced pathways even in the presence of extracellular high glucose concentration. This results in delayed cell proliferation, reduced ATP , induction of autophagy, and dephosphorylation of the TORC 1 substrates Atg13 and Sch9.