Chk2 homolog Mek1 limits exonuclease 1-dependent DNA end resection during meiotic recombination in Saccharomyces cerevisiae.

IF 3.3 3区生物学 Q2 GENETICS & HEREDITY

Genetics Pub Date : 2024-09-04 DOI:10.1093/genetics/iyae112

Jennifer T Krystosek, Douglas K Bishop

引用次数: 0

Abstract

The conserved Rad2/XPG family 5'-3' exonuclease, exonuclease 1 (Exo1), plays many roles in DNA metabolism including during resolution of DNA double-strand breaks via homologous recombination. Prior studies provided evidence that the end resection activity of Exo1 is downregulated in yeast and mammals by Cdk1/2 family cyclin-dependent and checkpoint kinases, including budding yeast kinase Rad53 which functions in mitotic cells. Here, we provide evidence that the master meiotic kinase Mek1, a paralog of Rad53, limits 5'-3' single-strand resection at the sites of programmed meiotic DNA breaks. Mutational analysis suggests that the mechanism of Exo1 suppression by Mek1 differs from that of Rad53.

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Chk2 同源物 Mek1 限制了 S. cerevisiae 中减数分裂重组过程中 Exo1 依赖性 DNA 末端切除。

保守的 Rad2/XPG 家族 5'-3' 外切酶--外切酶 1（Exo1）在 DNA 代谢中发挥着多种作用，包括通过同源重组解决 DNA 双链断裂（DSB）。先前的研究提供的证据表明，在酵母和哺乳动物体内，Exo1 的末端重组活性受 Cdk1/2 家族依赖细胞周期蛋白和检查点激酶（包括在有丝分裂细胞中发挥作用的芽殖酵母激酶 Rad53）的调控。在这里，我们提供了证据，证明减数分裂主激酶 Mek1（Rad53 的旁系亲属）限制了程序性减数分裂 DNA 断裂位点的 5'-3' 单链切除。突变分析表明，Mek1抑制Exo1的机制不同于Rad53。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Genetics GENETICS & HEREDITY-

CiteScore

6.90

自引率

6.10%

发文量

177

审稿时长

1.5 months

期刊介绍： GENETICS is published by the Genetics Society of America, a scholarly society that seeks to deepen our understanding of the living world by advancing our understanding of genetics. Since 1916, GENETICS has published high-quality, original research presenting novel findings bearing on genetics and genomics. The journal publishes empirical studies of organisms ranging from microbes to humans, as well as theoretical work. While it has an illustrious history, GENETICS has changed along with the communities it serves: it is not your mentor''s journal. The editors make decisions quickly – in around 30 days – without sacrificing the excellence and scholarship for which the journal has long been known. GENETICS is a peer reviewed, peer-edited journal, with an international reach and increasing visibility and impact. All editorial decisions are made through collaboration of at least two editors who are practicing scientists. GENETICS is constantly innovating: expanded types of content include Reviews, Commentary (current issues of interest to geneticists), Perspectives (historical), Primers (to introduce primary literature into the classroom), Toolbox Reviews, plus YeastBook, FlyBook, and WormBook (coming spring 2016). For particularly time-sensitive results, we publish Communications. As part of our mission to serve our communities, we''ve published thematic collections, including Genomic Selection, Multiparental Populations, Mouse Collaborative Cross, and the Genetics of Sex.