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Cdc5p在DNA复制中的新作用。

A novel role for Cdc5p in DNA replication.

作者信息

Hardy C F, Pautz A

机构信息

Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.

出版信息

Mol Cell Biol. 1996 Dec;16(12):6775-82. doi: 10.1128/MCB.16.12.6775.

DOI:10.1128/MCB.16.12.6775
PMID:8943332
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC231680/
Abstract

DNA replication initiates from specific chromosomal sites called origins, and in the budding yeast Saccharomyces cerevisiae these sites are occupied by the origin recognition complex (ORC). Dbf4p is proposed to play a role in targeting the G1/S kinase Cdc7p to initiation complexes late in G1. We report that Dbf4p may also recruit Cdc5p to origin complexes. Cdc5p is a member of the Polo family of kinases that is required for the completion of mitosis. Cdc5p and Cdc7p each interact with a distinct domain of Dbf4p. cdc5-1 mutants have a plasmid maintenance defect that can be suppressed by the addition of multiple origins. cdc5-1 orc2-1 double mutants are synthetically lethal. Levels of Cdc5p were found to be cell cycle regulated and peaked in G2/M. These results suggest a role for Cdc5p and possibly Polo-like kinases at origin complexes.

摘要

DNA复制从称为起始点的特定染色体位点开始,在出芽酵母酿酒酵母中,这些位点被起始点识别复合物(ORC)占据。Dbf4p被认为在G1晚期将G1/S激酶Cdc7p靶向起始复合物中发挥作用。我们报告Dbf4p也可能将Cdc5p招募到起始复合物中。Cdc5p是有丝分裂完成所必需的Polo激酶家族的成员。Cdc5p和Cdc7p各自与Dbf4p的不同结构域相互作用。cdc5-1突变体具有质粒维持缺陷,可通过添加多个起始点来抑制。cdc5-1 orc2-1双突变体是合成致死的。发现Cdc5p的水平受细胞周期调节,并在G2/M期达到峰值。这些结果表明Cdc5p以及可能的Polo样激酶在起始复合物中发挥作用。

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本文引用的文献

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Mechanisms restricting DNA replication to once per cell cycle: MCMS, pre-replicative complexes and kinases.将DNA复制限制在每个细胞周期进行一次的机制:微小染色体维持蛋白、复制前复合体和激酶。
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