Zhou Changyin, Zhang Xue, Miao Yilong, Zhang Yu, Li Yu, Xiong Bo
College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China.
Sci Adv. 2021 Sep 24;7(39):eabg9335. doi: 10.1126/sciadv.abg9335.
During the S phase of mitosis, Sororin is recruited by acetylated Smc3 and stabilizes sister chromatid cohesion by counteracting the Wapl-Pds5 interaction. Thereafter, Sororin is phosphorylated during prophase and translocated to the cytoplasm, where its function remains poorly understood. Here, we report that Sororin acts as a regulator of meiotic G-M transition and spindle assembly in mammalian oocytes. Sororin is present in the nucleus of GV oocytes and becomes associated with the spindle apparatus during meiosis I in mice. Depletion of Sororin causes failure of GVBD due to inactivation of Cdk1 and defective spindle assembly because of reduced levels of Cyclin B2. We validate Sororin interactions with Cyclin B2 that protects it from destruction by APC, which drives M phase entry and bipolar spindle formation. Notably, the meiotic functions of Sororin are conserved among mammals. Together, our findings provide novel insights into the noncanonical role of Sororin in the resumption of meiosis and progression through meiosis I in mammalian oocytes.
在有丝分裂的S期，Sororin被乙酰化的Smc3招募，并通过抵消Wapl-Pds5相互作用来稳定姐妹染色单体的黏连。此后，Sororin在前期被磷酸化并转移至细胞质，其在细胞质中的功能仍知之甚少。在此，我们报道Sororin在哺乳动物卵母细胞中作为减数分裂G-M转换和纺锤体组装的调节因子发挥作用。Sororin存在于生发泡（GV）期卵母细胞的细胞核中，并在小鼠减数分裂I期与纺锤体装置相关联。Sororin的缺失会导致由于Cdk1失活而引起的生发泡破裂（GVBD）失败，以及由于细胞周期蛋白B2水平降低而导致的纺锤体组装缺陷。我们验证了Sororin与细胞周期蛋白B2的相互作用，该相互作用保护细胞周期蛋白B2不被后期促进复合物（APC）破坏，而APC驱动M期进入和双极纺锤体形成。值得注意的是，Sororin的减数分裂功能在哺乳动物中是保守的。总之，我们的研究结果为Sororin在哺乳动物卵母细胞减数分裂恢复和减数分裂I进程中的非经典作用提供了新的见解。
