...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cell Division >Kif18a regulates Sirt2-mediated tubulin acetylation for spindle organization during mouse oocyte meiosis
【24h】

Kif18a regulates Sirt2-mediated tubulin acetylation for spindle organization during mouse oocyte meiosis

机译：Kif18a调节Sirt2介导的微管蛋白乙酰化以促进小鼠卵母细胞减数分裂的纺锤体组织

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

During oocyte meiosis, the cytoskeleton dynamics, especially spindle organization, are critical for chromosome congression and segregation. However, the roles of the kinesin superfamily in this process are still largely unknown. In the present study, Kif18a, a member of the kinesin-8 family, regulated spindle organization through its effects on tubulin acetylation in mouse oocyte meiosis. Our results showed that Kif18a is expressed and mainly localized in the spindle region. Knock down of Kif18a caused the failure of first polar body extrusion, dramatically affecting spindle organization and resulting in severe chromosome misalignment. Further analysis showed that the disruption of Kif18a caused an increase in acetylated tubulin level, which might be the reason for the spindle organization defects after Kif18a knock down in oocyte meiosis, and the decreased expression of deacetylase Sirt2 was found after Kif18a knock down. Moreover, microinjections of tubulin K40R mRNA, which could induce tubulin deacetylation, protected the oocytes from the effects of Kif18a downregulation, resulting in normal spindle morphology in Kif18a-knock down oocytes. Taken together, our results showed that Kif18a affected Sirt2-mediated tubulin acetylation level for spindle organization during mouse oocyte meiosis. Our results not only revealed the critical effect of Kif18a on microtubule stability, but also extended our understanding of kinesin activity in meiosis.
机译：在卵母细胞减数分裂期间，细胞骨架动力学，特别是纺锤体组织，对染色体的聚集和分离至关重要。但是，驱动蛋白超家族在这个过程中的作用仍然是未知的。在本研究中，Kif18a是kinesin-8家族的成员，通过其对小鼠卵母细胞减数分裂中微管蛋白乙酰化的作用来调控纺锤体的组织。我们的结果表明，Kif18a表达并主要定位于纺锤体区域。击倒Kif18a导致第一次极体挤出失败，极大地影响纺锤体组织，并导致严重的染色体错位。进一步的分析表明，Kif18a的破坏引起乙酰化微管蛋白水平的升高，这可能是卵母细胞减数分裂中Kif18a敲低后纺锤体组织缺陷的原因，而Kif18a敲低后发现脱乙酰基酶Sirt2表达降低。此外，微管蛋白K40R mRNA的显微注射可诱导微管蛋白去乙酰化，从而保护卵母细胞免受Kif18a下调的影响，从而导致敲低Kif18a卵母细胞的纺锤体形态正常。两者合计，我们的结果表明，在小鼠卵母细胞减数分裂过程中，Kif18a影响了Sirt2介导的微管蛋白乙酰化水平，从而促进了纺锤体的组织形成。我们的结果不仅揭示了Kif18a对微管稳定性的关键作用，而且扩展了我们对减数分裂中驱动蛋白活性的了解。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号