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首页> 外文期刊>Genome >Evidence that the spindle assembly checkpoint does not regulate APC~(Fzy) activity in Drosophila female meiosis
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Evidence that the spindle assembly checkpoint does not regulate APC~(Fzy) activity in Drosophila female meiosis

机译：在果蝇雌性减数分裂中纺锤体装配检查点不能调节APC〜（Fzy）活性的证据

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摘要

The spindle assembly checkpoint (SAC) plays an important role in mitotic cells to sense improper chromosome attachment to spindle microtubules and to inhibit APC~(Fzy)-dependent destruction of cyclin B and Securin; consequent initiation of anaphase until correct attachments are made. In Drosophila, SAC genes have been found to play a role in ensuring proper chromosome segregation in meiosis, possibly reflecting a similar role for the SAC in APC~(Fzy) inhibition during meiosis. We found that loss of function mutations in SAC genes, Mad2, zwilch, and mpsl, do not lead to the predicted rise in APC~(Fzy)-dependent degradation of cyclin B either globally throughout the egg or locally on the meiotic spindle. Further, the SAC is not responsible for the inability of APC~(Fzy) to target cyclin B and promote anaphase in metaphase H arrested eggs from cort mutant females. Our findings support the argument that SAC proteins play checkpoint independent roles in Drosophila female meiosis and that other mechanisms must function to control APC activity.
机译：纺锤体装配检查点（SAC）在有丝分裂细胞中起着重要的作用，以检测不正确的染色体与纺锤体微管的附着并抑制APC〜（Fzy）依赖性细胞周期蛋白B和Securin的破坏。随后开始后期，直到建立正确的附件。在果蝇中，已发现SAC基因在确保减数分裂中染色体的正确分离中起作用，这可能反映了SAC在减数分裂过程中在APC〜（Fzy）抑制中的相似作用。我们发现，SAC基因，Mad2，zwilch和mpsl中功能性突变的丧失并不会导致整个卵子中或减数分裂纺锤体上APC〜（Fzy）依赖性细胞周期蛋白B降解的增加。此外，SAC不负责使APC_（Fzy）无法靶向细胞周期蛋白B并促进来自cort突变雌性的中期H逮捕卵中的后期阶段。我们的发现支持以下论点：SAC蛋白在果蝇雌性减数分裂中发挥关卡独立的作用，并且其他机制必须起作用以控制APC活性。

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