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mik1(+) G1-S转录调控裂殖酵母中的有丝分裂进入。

mik1(+) G1-S transcription regulates mitotic entry in fission yeast.

作者信息

Ng S S, Anderson M, White S, McInerny C J

机构信息

Division of Biochemistry and Molecular Biology, Institute of Biological and Life Sciences, University of Glasgow, Glasgow G12 8QQ, UK.

出版信息

FEBS Lett. 2001 Aug 17;503(2-3):131-4. doi: 10.1016/s0014-5793(01)02720-x.

Abstract

In the fission yeast Schizosaccharomyces pombe Mik1p, in combination with Wee1p, is an important inhibitor of mitosis through direct phosphorylation of Cdc2p. Here we present the observation that mik1(+) is transcribed during G1- and S-phase in normally dividing cells. mik1(+) transcription is regulated by the MCB-DSC1 system, which controls expression of other genes at the G1-S interval. mik1(+) is shown to be an important target of MCB-DSC1 as it is epistatic for the mitotic delay phenotype displayed in cdc10-C4 cells, which are mutated in a component of DSC1. The mitotic delay in cdc10-C4 cells is bypassed by cdc2-1w, suggesting that mik1(+) acts directly on cdc2(+), with no checkpoint function involved. Thus, mik1(+) represents a new type of MCB-DSC1 regulated gene in fission yeast, whose gene product is exclusively expressed during G1- and S-phase to prevent premature mitosis during this cell cycle stage.

摘要

在裂殖酵母粟酒裂殖酵母中,Mik1p与Wee1p共同作用,通过直接磷酸化Cdc2p成为有丝分裂的重要抑制剂。在此,我们发现正常分裂细胞中mik1(+)在G1期和S期转录。mik1(+)转录受MCB-DSC1系统调控,该系统在G1-S间期控制其他基因的表达。mik1(+)被证明是MCB-DSC1的重要靶点,因为它对于在DSC1的一个组分中发生突变的cdc10-C4细胞所表现出的有丝分裂延迟表型是上位性的。cdc2-1w可绕过cdc10-C4细胞中的有丝分裂延迟,这表明mik1(+)直接作用于cdc2(+),不涉及检查点功能。因此,mik1(+)代表了裂殖酵母中一种新型的受MCB-DSC1调控的基因,其基因产物仅在G1期和S期表达,以防止在该细胞周期阶段过早进行有丝分裂。

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