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The Journal of biological chemistry v.292 no.7, 2017년, pp.2660 - 2669   SCI SCIE
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General Control Nonderepressible 2 (GCN2) Kinase Inhibits Target of Rapamycin Complex 1 in Response to Amino Acid Starvation in Saccharomyces cerevisiae

Yuan, Wenjie (From the School of Life Science and Biotechnology, Dalian University of Technology, Dalian 116024, China, ) ; Guo, Shuguang (the Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, and ) ; Gao, Jiaoqi (From the School of Life Science and Biotechnology, Dalian University of Technology, Dalian 116024, China, ) ; Zhong, Mingming (the Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, and ) ; Yan, Gonghong (the Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, and ) ; Wu, Wangmeng (the Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, and ) ; Chao, Yapeng (the State Key Laboratories of Transducer Technology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China ) ; Jiang, Yu (the Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburg ) ;
  • 초록  

    In eukaryotic cells, two conserved protein kinases, Gcn2 and TOR complex 1 (TORC1), couple amino acid conditions to protein translation. Gcn2 functions as an amino acid sensor and is activated by uncharged tRNAs that accumulate when intracellular amino acids are limited. Activated Gcn2 phosphorylates and inhibits eukaryotic initiation factor-2α (eIF2α), resulting in repression of general protein synthesis. Like Gcn2, TORC1 is also involved in sensing amino acid conditions. However, the underlying mechanism remains unclear. In the present study, we show that TORC1 is a direct target of Gcn2 kinase in the yeast Saccharomyces cerevisiae . In response to amino acid starvation, Gcn2 binds to TORC1 and phosphorylates Kog1, the unique regulatory subunit of TORC1, resulting in down-regulation of TORC1 kinase activity. In the absence of Gcn2, TORC1 signaling activity increases and becomes unresponsive to amino acid starvation. Our findings demonstrate that TORC1 is an effector of Gcn2 in amino acid signaling, hence defining a novel mechanism by which TORC1 senses amino acid starvation.


  • 주제어

    amino acid .   autophagy .   histidine .   TOR complex (TORC) .   yeast .   Gcn2 .   Kog1 .   TORC1 .   amino acid starvation .   uncharged tRNA.  

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