酿酒酵母G1期停滞期间甲硫氨酰转移核糖核酸缺乏

Methionyl-transfer ribonucleic acid deficiency during G1 arrest of Saccharomyces cerevisiae.

作者信息

Unger M W

出版信息

J Bacteriol. 1977 Apr;130(1):11-9. doi: 10.1128/jb.130.1.11-19.1977.

DOI:10.1128/jb.130.1.11-19.1977

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC235168/

Abstract

The mesl- mutants of Saccharomyces cerevisiae cease division and accumulate in the G1 interval of the cell cycle when deprived of methionine or shifted from 23 to 36 degrees C in the presence of methionine. Synchronous cell cycle arrest results from a deficiency of charged methionyl-transfer ribonucleic acid (methionyl-tRNAMet) as shown by direct measurement of the in vivo pools of methionine, S-adenosylmethionine, and methionyl-tRNAMet. The deficiency of methionyl-tRNAMet in these cells is the consequence of a lesion in a single gene, mes1. mes1 appears to be the structural gene for the methionyl-tRNA synthetase because some revertants of this mutation exhibited a thermolabile methionyl-tRNA synthetase in vitro. A sufficient hypothesis to explain these and previous results is that the control of cell division by S. cerevisiae in response to nutrient limitation is mediated through aminoacyl-tRNA or subsequent steps in protein biosynthesis.

摘要

酿酒酵母的mesl-突变体在缺乏甲硫氨酸或在有甲硫氨酸存在的情况下从23℃转移到36℃时，会停止分裂并在细胞周期的G1期积累。如通过直接测量体内甲硫氨酸、S-腺苷甲硫氨酸和甲硫氨酰-tRNA Met库所示，同步细胞周期停滞是由于甲硫氨酰转移核糖核酸（甲硫氨酰-tRNA Met）缺乏所致。这些细胞中甲硫氨酰-tRNA Met的缺乏是单个基因mes1发生损伤的结果。mes1似乎是甲硫氨酰-tRNA合成酶的结构基因，因为该突变的一些回复突变体在体外表现出热不稳定的甲硫氨酰-tRNA合成酶。一个足以解释这些及先前结果的假说是，酿酒酵母对营养限制作出反应时对细胞分裂的控制是通过氨酰-tRNA或蛋白质生物合成的后续步骤介导的。

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本文引用的文献

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Methionine-and S-adenosyl methionine-mediated repression in a methionyl-transfer ribonucleic-acid synthetase mutant of Saccharomyces cerevisiae.甲硫氨酸和S-腺苷甲硫氨酸介导的酿酒酵母甲硫氨酰转移核糖核酸合成酶突变体中的阻遏作用。

J Bacteriol. 1975 Aug;123(2):428-35. doi: 10.1128/jb.123.2.428-435.1975.

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