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Reduced dosage of the chromosome axis factor Red1 selectively disrupts the meiotic recombination checkpoint in Saccharomyces cerevisiae

机译:减少剂量的染色体轴因子Red1选择性地破坏了酿酒酵母中的减数分裂重组检查点

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摘要

Meiotic chromosomes assemble characteristic “axial element” structures that are essential for fertility and provide the chromosomal context for meiotic recombination, synapsis and checkpoint signaling. Whether these meiotic processes are equally dependent on axial element integrity has remained unclear. Here, we investigated this question in S. cerevisiae using the putative condensin allele ycs4S. We show that the severe axial element assembly defects of this allele are explained by a linked mutation in the promoter of the major axial element gene RED1 that reduces Red1 protein levels to 20–25% of wild type. Intriguingly, the Red1 levels of ycs4S mutants support meiotic processes linked to axis integrity, including DNA double-strand break formation and deposition of the synapsis protein Zip1, at levels that permit 70% gamete survival. By contrast, the ability to elicit a meiotic checkpoint arrest is completely eliminated. This selective loss of checkpoint function is supported by a RED1 dosage series and is associated with the loss of most of the cytologically detectable Red1 from the axial element. Our results indicate separable roles for Red1 in building the structural axis of meiotic chromosomes and mounting a sustained recombination checkpoint response.
机译:减数分裂染色体装配了对于生育力必不可少的特征性“轴向元件”结构,并为减数分裂重组,突触和检查点信号传递提供了染色体背景。这些减数分裂过程是否同样取决于轴向元素的完整性尚不清楚。在这里,我们使用推测的凝缩素等位基因ycs4S在酿酒酵母中调查了这个问题。我们表明,该等位基因的严重轴向元件装配缺陷是由主要轴向元件基因RED1启动子中的连锁突变所解释的,该突变将Red1蛋白水平降低至野生型的20–25%。有趣的是,ycs4S突变体的Red1水平支持与轴完整性相关的减数分裂过程,包括DNA双链断裂的形成和突触蛋白Zip1的沉积,其水平允许配子存活70%。相反,完全消除了减数分裂检查点停滞的能力。 RED1剂量系列支持这种检查点功能的选择性丧失,并且与轴向元件中大多数可细胞学检测的Red1丧失有关。我们的结果表明Red1在建立减数分裂染色体的结构轴和建立持续的重组检查点反应中具有可分离的作用。

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