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Spindle assembly checkpoint proteins regulate and monitor meiotic synapsis in C. elegans

机译:纺锤体装配检查点蛋白调节和监测秀丽隐杆线虫的减数分裂突触

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摘要

Homologue synapsis is required for meiotic chromosome segregation, but how synapsis is initiated between chromosomes is poorly understood. In Caenorhabditis elegans, synapsis and a checkpoint that monitors synapsis depend on pairing centers (PCs), cis-acting loci that interact with nuclear envelope proteins, such as SUN-1, to access cytoplasmic microtubules. Here, we report that spindle assembly checkpoint (SAC) components MAD-1, MAD-2, and BUB-3 are required to negatively regulate synapsis and promote the synapsis checkpoint response. Both of these roles are independent of a conserved component of the anaphase-promoting complex, indicating a unique role for these proteins in meiotic prophase. MAD-1 and MAD-2 localize to the periphery of meiotic nuclei and interact with SUN-1, suggesting a role at PCs. Consistent with this idea, MAD-1 and BUB-3 require full PC function to inhibit synapsis. We propose that SAC proteins monitor the stability of pairing, or tension, between homologues to regulate synapsis and elicit a checkpoint response.
机译:同源突触是减数分裂染色体分离所必需的,但是人们对染色体之间如何突触的了解却很少。在秀丽隐杆线虫中,突触和监测突触的检查点取决于配对中心(PCs),即与核包膜蛋白(例如SUN-1)相互作用的顺式作用位点,以进入胞质微管。在这里,我们报告主轴组件检查点(SAC)组件MAD-1,MAD-2和BUB-3需要负调节突触并促进突触检查点响应。这两个角色均独立于后期促进复合物的保守成分,表明这些蛋白质在减数分裂前期中的独特作用。 MAD-1和MAD-2定位于减数分裂核的外围,并与SUN-1相互作用,提示在PC上发挥作用。与此想法一致,MAD-1和BUB-3需要完整的PC功能来抑制突触。我们建议SAC蛋白监视同源之间的配对或张力的稳定性,以调节突触并引发检查点反应。

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