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SCF 泛素连接酶在减数分裂过程中调节联会复合体的形成。

SCF ubiquitin ligase regulates synaptonemal complex formation during meiosis.

机构信息

Institute for Protein Research, Osaka University, Suita, Osaka, Japan.

出版信息

Life Sci Alliance. 2020 Dec 8;4(2). doi: 10.26508/lsa.202000933. Print 2021 Feb.

Abstract

Homologous chromosomes pair with each other during meiosis, culminating in the formation of the synaptonemal complex (SC), which is coupled with meiotic recombination. In this study, we showed that a meiosis-specific depletion mutant of a cullin (Cdc53) in the SCF (Skp-Cullin-F-box) ubiquitin ligase, which plays a critical role in cell cycle regulation during mitosis, is deficient in SC formation. However, the mutant is proficient in forming crossovers, indicating the uncoupling of meiotic recombination with SC formation in the mutant. Furthermore, the deletion of the gene encoding a meiosis-specific AAA+ ATPase suppresses SC-assembly defects induced by depletion. On the other hand, the double mutant is defective in meiotic crossover formation, suggesting the assembly of SC with unrepaired DNA double-strand breaks. A temperature-sensitive mutant of , which encodes an F-box protein of SCF, shows meiotic defects similar to those of the -depletion mutant. These results suggest that SCF, probably SCF-dependent protein ubiquitylation, regulates and collaborates with Pch2 in SC assembly and meiotic recombination.

摘要

在减数分裂过程中,同源染色体相互配对,最终形成联会复合体(SC),这与减数分裂重组相偶联。在这项研究中,我们表明,在 SCF(Skp-Cullin-F-box)泛素连接酶中,一个减数分裂特异性的 Cullin(Cdc53)耗竭突变体,在有丝分裂期间的细胞周期调控中发挥关键作用,其 SC 形成缺陷。然而,该突变体在形成交叉方面是高效的,表明在该突变体中减数分裂重组与 SC 形成的解偶联。此外,缺失编码一个减数分裂特异性 AAA+ATP 酶的 基因可抑制由 耗竭引起的 SC 组装缺陷。另一方面, 双突变体在减数分裂交叉形成中是有缺陷的,这表明 SC 与未修复的 DNA 双链断裂的组装。SCF 的一个温度敏感突变体,其编码 SCF 的 F-box 蛋白,显示出与 -耗竭突变体相似的减数分裂缺陷。这些结果表明,SCF 可能是 SCF 依赖性蛋白泛素化,调节和与 Pch2 合作参与 SC 组装和减数分裂重组。

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