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Cyclin A2 is required for sister chromatid segregation, but not separase control, in mouse oocyte meiosis.

机译:在小鼠卵母细胞减数分裂中,姊妹染色单体分离(而不是分离酶控制)需要细胞周期蛋白A2。

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摘要

In meiosis, two specialized cell divisions allow the separation of paired chromosomes first, then of sister chromatids. Separase removes the cohesin complex holding sister chromatids together in a stepwise manner from chromosome arms in meiosis I, then from the centromere region in meiosis II. Using mouse oocytes, our study reveals that cyclin A2 promotes entry into meiosis, as well as an additional unexpected role; namely, its requirement for separase-dependent sister chromatid separation in meiosis II. Untimely cyclin A2-associated kinase activity in meiosis I leads to precocious sister separation, whereas inhibition of cyclin A2 in meiosis II prevents it. Accordingly, endogenous cyclin A is localized to kinetochores throughout meiosis II, but not in anaphase I. Additionally, we found that cyclin B1, but not cyclin A2, inhibits separase in meiosis I. These findings indicate that separase-dependent cohesin removal is differentially regulated by cyclin B1 and A2 in mammalian meiosis.
机译:在减数分裂中,两个专门的细胞分裂允许首先分离配对的染色体,然后分离姊妹染色单体。 Separase从减数分裂I的染色体臂,然后从减数分裂II的着丝粒区域中逐步除去粘附姐妹染色单体的凝聚素复合物。使用小鼠卵母细胞,我们的研究表明细胞周期蛋白A2促进减数分裂的进入,以及其他意外作用。即它对减数分裂II中分离酶依赖性姐妹染色单体分离的要求。减数分裂I中与细胞周期蛋白A2相关的激酶活性过早导致姐妹早熟分离,而减数分裂II中细胞周期蛋白A2的抑制阻止了它的发生。因此,内源性细胞周期蛋白A定位于整个减数分裂II的动植物,而不是在后期I。此外,我们发现细胞周期蛋白B1而不是细胞周期蛋白A2抑制减数分裂I的分离酶。这些发现表明分离酶依赖的粘着蛋白去除受到不同的调节细胞周期蛋白B1和A2在哺乳动物减数分裂中的作用

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