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首页> 外文期刊>Cell cycle >Analysis of Polo-like kinase Cdc5 in the meiosis recombination checkpoint.
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Analysis of Polo-like kinase Cdc5 in the meiosis recombination checkpoint.

机译：分裂重组检查点中鼠标样激酶CDC5分析。

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摘要

In meiosis, accumulation of recombination intermediates or defects in chromosome synapsis trigger checkpoint-mediated arrest in prophase I. Such 'checkpoints' are important surveillance mechanisms that ensure temporal dependence of cell cycle events. The budding yeast Polo-like kinase, Cdc5, has been identified as a key regulator of the meiosis I chromosome segregation pattern. Here we have analysed the role of Cdc5 in the recombination checkpoint and observed that Polo-like kinase is not required for checkpoint activation in yeast meiosis. Surprisingly, depletion of CDC5 in the Deltarad17 checkpoint-defective background resulted in nuclear fragmentation to levels even higher than that observed in Deltadmc1 Deltarad17 cells that bypass the checkpoint arrest despite accumulating DNA double-strand breaks. The spindle morphology of Cdc5-depleted cells included short, thick metaphase I spindles in mononucleate cells and disassembled spindles in binucleate and tetranucleate cells, although this phenotype does not appear to be the cause of the nuclear fragmentation. An exaggeration of chromosome synapsis defects occurred in Cdc5-depleted Deltarad17 cells and may contribute to the nuclear fragmentation phenotype. The analysis also uncovered a role for Cdc5 in maintaining spindle integrity in Deltadmc1 Deltarad17 cells. Further analysis confirmed that adaptation to DNA damage does occur in meiosis and that CDC5 is required for this process. The cdc5-ad mutation that renders cells unable to adapt to DNA damage in mitosis did not affect checkpoint adaptation in meiosis, indicating that the mechanisms of checkpoint adaptation in mitosis and meiosis are not fully conserved.
机译：在减数分裂中，复合中间体的积累或染色体突触触发检查点介导的逮捕中的重组中间体或缺陷在预言中。这些“检查点”是重要的监测机制，以确保细胞周期事件的时间依赖。已经鉴定为MeIosis i染色体隔离模式的关键调节剂的萌芽酵母Polo样激酶。在这里，我们已经分析了CDC5在重组检查点中的作用，并观察到酵母减数分裂中的检查点激活不需要POLO样激酶。令人惊讶的是，Deltarad17检查点缺陷背景下的CDC5耗尽导致核碎片甚至高于在Deltadmc1 Deltarad17细胞中观察到的水平，尽管积累DNA双链断裂，但仍然是逐步抑制的细胞。 CDC5耗尽细胞的主轴形态包括短，厚的中磷酶I纺织在单核细胞中，拆卸在离子蛋白和四核细胞中的主轴，尽管这种表型似乎不是核碎裂的原因。 CDC5耗尽的Deltarad17细胞中发生染色体突触缺陷的夸张，可能有助于核碎片表型。该分析还发现CDC5在维持DeltadmC1 Deltarad17细胞中保持主轴完整性的作用。进一步的分析证实，在减数分裂中会发生对DNA损伤的适应，并且该过程需要CDC5。 CDC5-AD突变使细胞不能适应有丝分裂中的DNA损伤并不影响减数分裂中的检查点适应性，表明有丝分裂和减数分裂的检查点适应的机制并不完全保守。

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  • 来源
    《Cell cycle》 |2010年第6期|共12页
  • 作者

    Iacovella MG; Kelly JS; Clyne RK;

  • 作者单位

    UCD Conway Institute of Biomolecular &

    Biomedical Research and School of Biomolecular and Biomedical Science University College Dublin Belfield Dublin Ireland.;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;
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