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Chromosome-Wide Regulation of Meiotic Crossover Formation in Caenorhabditis elegans Requires Properly Assembled Chromosome Axes

机译:秀丽隐杆线虫减数分裂形成的染色体全域调节需要正确组装的染色体轴。

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摘要

Most sexually reproducing organisms depend on the regulated formation of crossovers, and the consequent chiasmata, to accomplish successful segregation of homologous chromosomes at the meiosis I division. A robust, chromosome-wide crossover control system limits chromosome pairs to one crossover in most meioses in the nematode Caenorhabditis elegans; this system has been proposed to rely on structural integrity of meiotic chromosome axes. Here, we test this hypothesis using a mutant, him-3(me80), that assembles reduced levels of meiosis-specific axis component HIM-3 along cohesin-containing chromosome axes. Whereas pairing, synapsis, and crossing over are eliminated when HIM-3 is absent, the him-3(me80) mutant supports assembly of synaptonemal complex protein SYP-1 along some paired chromosomes, resulting in partial competence for chiasma formation. We present both genetic and cytological evidence indicating that the him-3(me80) mutation leads to an increased incidence of meiotic products with two crossovers. These results indicate that limiting the amount of a major axis component results in a reduced capacity to communicate the presence of a (nascent) crossover and/or to discourage others in response.
机译:大多数有性生殖生物都依赖于交叉的调控形式以及随之而来的chiasmata,以在减数分裂I区成功完成同源染色体的分离。强大的全染色体交叉控制系统可将线虫秀丽隐杆线虫的大多数中型染色体的染色体对限制为一个交叉。已经提出该系统依赖于减数分裂染色体轴的结构完整性。在这里,我们使用突变体him-3(me80)检验了这一假设,该突变体沿含黏着蛋白的染色体轴组装了减数分裂相关的特定轴成分HIM-3。缺少HIM-3时,消除了配对,突触和交叉,而him-3(me80)突变体则支持突触复合蛋白SYP-1沿着某些成对的染色体装配,从而导致了部分as骨形成的能力。我们提供了遗传和细胞学证据,表明him-3(me80)突变导致减数分裂产物的发生率增加,发生两次交叉。这些结果表明,限制主轴分量的数量会导致通信(新生)分频器和/或阻止其他人响应的能力降低。

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