Fission yeast Pib2 localizes to vacuolar membranes and regulates TOR complex 1 through evolutionarily conserved domains

被引:0
作者
Morozumi, Yuichi [1 ]
Hayashi, Yumi [1 ]
Chu, Cuong Minh [1 ]
Sofyantoro, Fajar [1 ,2 ]
Akikusa, Yutaka [1 ]
Fukuda, Tomoyuki [3 ]
Shiozaki, Kazuhiro [1 ,4 ]
机构
[1] Nara Inst Sci & Technol, Div Biol Sci, Ikoma, Nara 6300192, Japan
[2] Univ Gadjah Mada, Fac Biol, Dept Anim Physiol, Yogyakarta, Indonesia
[3] Niigata Univ, Grad Sch Med & Dent Sci, Dept Cellular Physiol, Niigata, Japan
[4] Univ Calif Davis, Dept Microbiol & Mol Genet, Davis, CA USA
基金
日本学术振兴会;
关键词
fission yeast; Pib2; TOR complex 1; vacuolar membrane; RAG GTPASES; PROTEIN; GROWTH; RHEB; KINASE; ACTIVATION; MTORC1; IDENTIFICATION; RAGULATOR; GLUTAMINE;
D O I
10.1002/1873-3468.14980
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
TOR complex 1 (TORC1) is a multi-protein kinase complex that coordinates cellular growth with environmental cues. Recent studies have identified Pib2 as a critical activator of TORC1 in budding yeast. Here, we show that loss of Pib2 causes severe growth defects in fission yeast cells, particularly when basal TORC1 activity is diminished by hypomorphic mutations in tor2, the gene encoding the catalytic subunit of TORC1. Consistently, TORC1 activity is significantly compromised in the tor2 hypomorphic mutants lacking Pib2. Moreover, as in budding yeast, fission yeast Pib2 localizes to vacuolar membranes via its FYVE domain, with its tail motif indispensable for TORC1 activation. These results strongly suggest that Pib2-mediated positive regulation of TORC1 is evolutionarily conserved between the two yeast species.
引用
收藏
页码:2886 / 2896
页数:11
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