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Study on simultaneous yet independent regulation of actin cytoskeletal organization and translation initiation by environmental stress

环境应激对肌动蛋白细胞骨架组织和翻译起始的同步但独立调控的研究

基本信息

批准号：
15570142
负责人：
UESONO Yukifumi
金额：
$ 1.92万
依托单位：
The University of Tokyo
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2003
资助国家：
日本
起止时间：
2003 至 2004
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-15570142/
关键词：
Osmolarity Glucose Actin Protein synthesis Stress Environment Signal transduction 翻訳

项目摘要

Acute glucose deprivation rapidly but transiently depolarizes the actin cytoskeleton and inhibits translation initiation in Saccharomyces cerevisiae. Neither rapid actin depolarization nor translation inhibition upon glucose removal occurs in a reg1 disruptant, which is defective in glucose repression, or in the tpk1^w mutant, which has weak cAPK activity. In the absence of additional glucose, recovery of either actin polarization or translation initiation relies upon respiration, the Snf1p protein kinase, and the transcription factors Msn2p and Msn4p. The readdition of glucose to glucose-starved cells causes a rapid recovery of actin polarization as well as translation initiation without respiration. These results indicate that the simultaneous regulation of actin polarization and translation initiation is divided into three reactions : (1)rapid shutdown depending on Reg1p and cAPK after glucose removal, (2)slow adaptation depending on Snf1p and Msn2p/4p in the absence of glucose, and (3)rapid recovery upon readdition of glucose. Upon glucose removal, translation initiation is rapidly inhibited in a rom2 disruptant, which is defective in rapid actin depolarization, whereas rapid actin depolarization occurs in a pop2/caf1 disruptant, which is defective in rapid inhibition of translation initiation. Thus, translation initiation and actin polarization appear to be simultaneously but independently regulated by glucose deprivation.

急性葡萄糖剥夺迅速但短暂地使肌动蛋白细胞骨架去极化并抑制酿酒酵母的翻译起始。在葡萄糖阻遏缺陷的reg 1破坏物或cAPK活性弱的tpk1^w突变体中，葡萄糖去除后既不发生快速肌动蛋白去极化，也不发生翻译抑制。在没有额外的葡萄糖的情况下，无论是肌动蛋白极化或翻译起始的恢复依赖于呼吸，Snf 1 p蛋白激酶，和转录因子Msn 2 p和Msn 4p。葡萄糖的再添加到葡萄糖饥饿的细胞引起肌动蛋白极化的快速恢复以及翻译起始而没有呼吸。这些结果表明，肌动蛋白极化和翻译起始的同时调节分为三个反应：（1）快速关闭依赖于Reg 1 p和cAPK在葡萄糖去除后，（2）缓慢适应依赖于Snf 1 p和Msn 2 p/4p在葡萄糖缺乏时，和（3）快速恢复后，再加入葡萄糖。在葡萄糖去除后，翻译起始在rom 2破坏剂中被快速抑制，这是在快速肌动蛋白去极化缺陷，而快速肌动蛋白去极化发生在pop 2/caf 1破坏剂中，这是在翻译起始的快速抑制缺陷。因此，翻译起始和肌动蛋白极化似乎是同时，但独立的葡萄糖剥夺调节。