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Meiotic checkpoints and the interchromosomal effect on crossing over in Drosophila females

机译:果蝇雌性的减数分裂检查点和染色体间作用对交叉的影响

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摘要

During prophase of meiosis I, genetic recombination is initiated with a Spo11-dependent DNA double-strand break (DSB). Repair of these DSBs can generate crossovers, which become chiasmata and are important for the process of chromosome segregation. To ensure at least one chiasma per homologous pair of chromosomes, the number and distribution of crossovers is regulated. One system contributing to the distribution of crossovers is the pachytene checkpoint, which requires the conserved gene pch2 that encodes an AAA+ATPase family member. Pch2-dependent pachytene checkpoint function causes delays in pachytene progression when there are defects in processes required for crossover formation, such as mutations in DS B-repair genes and when there are defects in the structure of the meiotic chromosome axis. Thus, the pachytene checkpoint appears to monitor events leading up to the generation of crossovers. Interestingly, heterozygous chromosome rearrangements cause Pch2-dependent pachytene delays and as little as two breaks in the continuity of the paired chromosome axes are sufficient to evoke checkpoint activity. These chromosome rearrangements also cause an interchromosomal effect on recombination whereby crossing over is suppressed between the affected chromosomes but is increased between the normal chromosome pairs. We have shown that this phenomenon is also due to pachytene checkpoint activity.
机译:在减数分裂I的前期,通过Spo11依赖的DNA双链断裂(DSB)启动基因重组。这些DSB的修复会产生交叉,该交叉变成Chiasmata,对于染色体分离过程很重要。为了确保每个同源染色体对至少有一个交叉,调节了交叉的数量和分布。一种促进交叉分布的系统是粗线检查点,其需要保守的基因pch2,该基因编码AAA + ATPase家族成员。当交叉形成所需的过程中存在缺陷(例如DS B修复基因中的突变)并且减数分裂染色体轴的结构存在缺陷时,依赖Pch2的粗线检查点功能会导致线粒体进程延迟。因此,粗线检查点似乎监视导致交叉产生的事件。有趣的是,杂合染色体重排导致Pch2依赖的粗线延迟,而成对染色体轴的连续性中只有两个断裂足以引起检查点活性。这些染色体重排还会对重组产生染色体间效应,从而在受影响的染色体之间抑制交叉,但在正常染色体对之间增加交叉。我们已经表明,这种现象也归因于粗线烯检查站的活动。

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