生物
减数分裂II
细胞周期蛋白依赖激酶1
细胞生物学
减数分裂
细胞周期蛋白B
卵母细胞
细胞周期蛋白
细胞周期蛋白B1
卵母细胞激活
促成熟因子
细胞周期蛋白
细胞周期检查点
细胞周期
遗传学
胚胎
细胞
基因
作者
Nora Bouftas,Lena Schneider,Marc Halder,Rebecca Demmig,Martina Baack,Damien Cladière,Melanie Walter,Hiba Al Abdallah,Camilla Kleinhempel,Ria Messaritaki,Janina Müller,Francesca Passarelli,Patrick Wehrle,Andreas Heim,Katja Wassmann,Thomas U. Mayer
标识
DOI:10.1016/j.devcel.2022.09.005
摘要
To ensure successful offspring ploidy, vertebrate oocytes must halt the cell cycle in meiosis II until sperm entry. Emi2 is essential to keep oocytes arrested until fertilization. However, how this arrest is implemented exclusively in meiosis II and not prematurely in meiosis I has until now remained enigmatic. Using mouse and frog oocytes, we show here that cyclin B3, an understudied B-type cyclin, is essential to keep Emi2 levels low in meiosis I. Direct phosphorylation of Emi2 at an evolutionarily highly conserved site by Cdk1/cyclin B3 targets Emi2 for degradation. In contrast, Cdk1/cyclin B1 is inefficient in Emi2 phosphorylation, and this provides a molecular explanation for the requirement of different B-type cyclins for oocyte maturation. Cyclin B3 degradation at exit from meiosis I enables Emi2 accumulation and thus timely arrest in meiosis II. Our findings illuminate the evolutionarily conserved mechanisms that control oocyte arrest for fertilization at the correct cell-cycle stage, which is essential for embryo viability.
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