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CDK 对裂殖酵母减数分裂中 DSB 形成和重组的贡献。

CDK contribution to DSB formation and recombination in fission yeast meiosis.

机构信息

Instituto de Biología Funcional y Genómica, Consejo Superior de Investigaciones Científicas, Salamanca, Spain.

Instituto de Biología Funcional y Genómica and Departamento de Microbiología y Genética, Universidad de Salamanca, Salamanca, Spain.

出版信息

PLoS Genet. 2019 Jan 14;15(1):e1007876. doi: 10.1371/journal.pgen.1007876. eCollection 2019 Jan.

Abstract

CDKs (cyclin-dependent kinases) associate with different cyclins to form different CDK-complexes that are fundamental for an ordered cell cycle progression, and the coordination of this progression with different aspects of the cellular physiology. During meiosis programmed DNA double-strand breaks (DSBs) initiate recombination that in addition to generating genetic variability are essential for the reductional chromosome segregation during the first meiotic division, and therefore for genome stability and viability of the gametes. However, how meiotic progression and DSB formation are coordinated, and the role CDKs have in the process, is not well understood. We have used single and double cyclin deletion mutants, and chemical inhibition of global CDK activity using the cdc2-asM17 allele, to address the requirement of CDK activity for DSB formation and recombination in fission yeast. We report that several cyclins (Cig1, Cig2, and the meiosis-specific Crs1) control DSB formation and recombination, with a major contribution of Crs1. Moreover, complementation analysis indicates specificity at least for this cyclin, suggesting that different CDK complexes might act in different pathways to promote recombination. Down-regulation of CDK activity impinges on the formation of linear elements (LinEs, protein complexes required for break formation at most DSB hotspot sites). This defect correlates with a reduction in the capability of one structural component (Rec25) to bind chromatin, suggesting a molecular mechanism by which CDK controls break formation. However, reduction in DSB formation in cyclin deletion mutants does not always correspondingly correlate with a proportional reduction in meiotic recombination (crossovers), suggesting that specific CDK complexes might also control downstream events balancing repair pathways. Therefore, our work points to CDK regulation of DSB formation as a key conserved feature in the initiation of meiotic recombination, in addition to provide a view of possible roles CDK might have in other steps of the recombination process.

摘要

CDKs(细胞周期蛋白依赖性激酶)与不同的细胞周期蛋白结合形成不同的 CDK 复合物,这些复合物对于细胞周期的有序进展以及与细胞生理不同方面的协调至关重要。在减数分裂过程中,程序性 DNA 双链断裂(DSBs)引发重组,除了产生遗传变异性外,对于第一次减数分裂中的染色体减少分离也是必不可少的,因此对于基因组稳定性和配子的存活力也是必不可少的。然而,减数分裂的进展和 DSB 的形成是如何协调的,以及 CDK 在这个过程中的作用,还不是很清楚。我们使用了单个和双细胞周期蛋白缺失突变体,以及使用 cdc2-asM17 等位基因化学抑制全局 CDK 活性,来研究裂殖酵母中 CDK 活性对 DSB 形成和重组的要求。我们报告说,几种细胞周期蛋白(Cig1、Cig2 和减数分裂特异性的 Crs1)控制 DSB 的形成和重组,其中 Crs1 的贡献最大。此外,互补分析表明至少对于这种细胞周期蛋白具有特异性,这表明不同的 CDK 复合物可能在不同的途径中发挥作用以促进重组。CDK 活性的下调会影响线性元件(LinEs,大多数 DSB 热点位点断裂形成所需的蛋白质复合物)的形成。这个缺陷与一个结构成分(Rec25)结合染色质的能力降低有关,这表明了 CDK 控制断裂形成的分子机制。然而,在细胞周期蛋白缺失突变体中 DSB 形成的减少并不总是与减数分裂重组(交叉)的相应比例减少相关,这表明特定的 CDK 复合物也可能控制下游事件,平衡修复途径。因此,我们的工作表明 CDK 对 DSB 形成的调控是启动减数分裂重组的一个关键保守特征,此外还提供了 CDK 在重组过程的其他步骤中可能具有的作用的观点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71bc/6331086/8894f19dc78e/pgen.1007876.g001.jpg

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