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首页> 外文期刊>Cell cycle >Reduced ability to recover from spindle disruption and loss of kinetochore spindle assembly checkpoint proteins in oocytes from aged mice
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Reduced ability to recover from spindle disruption and loss of kinetochore spindle assembly checkpoint proteins in oocytes from aged mice

机译：恢复衰老小鼠卵母细胞中的纺锤体破坏和动线轴纺锤体装配检查点蛋白丢失的能力降低

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Currently, maternal aging in women, based on mouse models, is thought to raise oocyte aneuploidy rates, because chromosome cohesion deteriorates during prophase arrest, and Sgo2, a protector of centromeric cohesion, is lost. Here we show that the most common mouse strain, C57Bl6/J, is resistant to maternal aging, showing little increase in aneuploidy or Sgo2 loss. Instead it demonstrates significant kinetochore-associated loss in the spindle assembly checkpoint protein Mad2 and phosphorylated Aurora C, which is involved in microtubule-kinetochore error correction. Their loss affects the fidelity of bivalent segregation but only when spindle organization is impaired during oocyte maturation. These findings have an impact clinically regarding the handling of human oocytes ex vivo during assisted reproductive techniques and suggest there is a genetic basis to aneuploidy susceptibility.
机译：目前，基于小鼠模型的妇女产妇衰老被认为会提高卵母细胞的非整倍性率，因为染色体的内聚力在前期停滞期间会恶化，并且会丢失着丝粒内聚力的保护因子Sgo2。在这里，我们显示最常见的小鼠品系C57B16 / J对母体衰老具有抗性，在非整倍性或Sgo2丢失方面几乎没有增加。相反，它表明纺锤体装配检查点蛋白Mad2和磷酸化的Aurora C显着与动线相关的损失，这涉及微管-动线错误校正。它们的损失影响二价分离的保真度，但仅在卵母细胞成熟过程中纺锤体组织受损时才会发生。这些发现对辅助生殖技术中离体人卵母细胞的处理具有临床影响，并提示非整倍性易感性具有遗传基础。

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