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首页> 外文期刊>Genetics >Rtf1-Mediated Eukaryotic Site-Specific Replication Termination
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Rtf1-Mediated Eukaryotic Site-Specific Replication Termination

机译:Rtf1介导的真核位点特异性复制终止

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摘要

High-fidelity chromosome segregation requires that the sister chromatids produced during S phase alsonbecome paired during S phase. Ctf7p (Eco1p) is required to establish sister chromatid pairing specificallynduring DNA replication. However, Ctf7p also becomes active during G2/M in response to DNA damage.nCtf7p is a phosphoprotein and an in vitro target of Cdc28p cyclin-dependent kinase (CDK), suggesting onenpossible mechanism for regulating the essential function of Ctf7p. Here, we report a novel synthetic lethalninteraction between ctf7 and cdc28. However, neither elevated CDC28 levels nor CDC28 Cak1p-bypass allelesnrescue ctf7 cell phenotypes. Moreover, cells expressing Ctf7p mutated at all full- and partial-consensus CDKphosphorylationnsites exhibit robust cell growth. These and other results reveal that Ctf7p regulation is morencomplicated than previously envisioned and suggest that CDK acts in sister chromatid cohesion parallel tonCtf7p reactions.
机译:高保真染色体分离要求在S期产生的姐妹染色单体也必须成对。需要Ctf7p(Eco1p)建立专门染色DNA复制的姐妹染色单体配对。然而,Ctf7p在G2 / M期间也能响应DNA损伤而变得活跃.nCtf7p是一种磷蛋白,是Cdc28p细胞周期蛋白依赖性激酶(CDK)的体外靶标,提示了调节Ctf7p基本功能的可能机制。在这里,我们报告ctf7和cdc28之间的新型合成致死相互作用。但是,既没有升高的CDC28水平,也没有CDC28 Cak1p旁路等位基因拯救ctf7细胞表型。此外,表达在所有完全和部分共识的CDK磷酸化位点处突变的Ctf7p的细胞均表现出强劲的细胞生长。这些和其他结果表明,Ctf7p调控比以前设想的要复杂得多,并且表明CDK在姐妹染色单体内聚平行tonCtf7p反应中起作用。

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