脱基酶USP8调节了卵细胞中的螺旋组装检查点
Changyin Zhou 周长银1, Xue Zhang 张雪1, Genlu Xu 许根露1
1Guangzhou Key Laboratory of Metabolic Diseases and Reproductive Health, Guangdong-Hong Kong Metabolism & Reproduction Joint Laboratory, Reproductive Medicine Center, The Affiliated Guangdong Second Provincial General Hospital of Jinan University, Guangzhou 510317, China.
Science advances
|March 13, 2026
概括
双基因酶USP8调节卵细胞中的螺旋组合检查点 (SAC),防止无倍积分. USP8稳定BUB3,一个关键的SAC蛋白,以确保适当的染色体对齐和卵形成.
科学领域:
- 细胞生物学 细胞生物学
- 生殖生物学 生殖生物学
- 遗传学 是一个遗传学.
背景情况:
- 螺旋组合检查点 (SAC) 对于预防卵细胞的无菌体积,这与不孕症和发育障碍有关,至关重要.
- 在 oogenesis 期间 SAC 调节中 deubiquitination 的作用仍然在很大程度上未被探索.
研究的目的:
- 为了调查duebiquitination在卵细胞内的SAC调节中的参与.
- 为了确定特定的duebiquitinases,可以调节SAC功能,并防止动脉积分.
主要方法:
- 卵细胞中USP8 (ubiquitin特定蛋白酶8) 的耗尽.
- 分析介质性进展,螺旋组合和染色体对齐.
- 免疫沉以确定蛋白质相互作用.
- 评估BUB3 (由胺醇3不抑制的布丁) 的稳定性和功能.
主要成果:
- 由于USP8的耗尽,SAC被禁用,导致中位分裂加速和异常的染色体分离.
- USP8通过其二化活性与BUB3相互作用并稳定BUB3,这是一个关键的SAC成分.
- 过度表达BUB3可挽救USP8贫卵细胞中的阳性积分缺陷.
结论:
- 脱化,特别是通过USP8,是卵细胞中SAC的关键调节机制.
- 通过稳定BUB3,USP8可以防止体卵形成,突出显示了它在卵细胞质量控制中的新作用.
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