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裂殖酵母Pib2定位于液泡膜,并通过进化保守结构域调节TOR复合体1。

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

作者信息

Morozumi Yuichi, Hayashi Yumi, Chu Cuong Minh, Sofyantoro Fajar, Akikusa Yutaka, Fukuda Tomoyuki, Shiozaki Kazuhiro

机构信息

Division of Biological Science, Nara Institute of Science and Technology, Ikoma, Japan.

Department of Animal Physiology, Faculty of Biology, Universitas Gadjah Mada, Yogyakarta, Indonesia.

出版信息

FEBS Lett. 2024 Dec;598(23):2886-2896. doi: 10.1002/1873-3468.14980. Epub 2024 Jul 15.

Abstract

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.

摘要

TOR复合物1(TORC1)是一种多蛋白激酶复合物,它能根据环境信号协调细胞生长。最近的研究已确定Pib2是芽殖酵母中TORC1的关键激活因子。在此,我们表明Pib2的缺失会导致裂殖酵母细胞出现严重的生长缺陷,尤其是当TORC1的基础活性因tor2(编码TORC1催化亚基的基因)的亚效突变而降低时。同样,在缺乏Pib2的tor2亚效突变体中,TORC1活性显著受损。此外,与芽殖酵母一样,裂殖酵母的Pib2通过其FYVE结构域定位于液泡膜,其尾部基序对于TORC1激活不可或缺。这些结果有力地表明,Pib2介导的对TORC1的正向调控在这两种酵母物种之间具有进化保守性。

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