细胞生物学
动细胞
微管
驱动蛋白
有丝分裂
主轴装置
生物
卵母细胞
减数分裂
染色体分离
主轴检查点
细胞分裂
遗传学
细胞
胚胎
染色体
基因
作者
Wei Wang,Zhanqun Shi,D. Zhang,Wenwen Hou,Huijie Ma,X Z Liu,Yongteng Zhang,Jinbao Zhu,Zhongju Yang,Bo Jia,Qimei Xu,Yunhai Zhang,Mianqun Zhang
标识
DOI:10.1096/fj.202400989r
摘要
Abstract Kif16A, a member of the kinesin‐3 family of motor proteins, has been shown to play crucial roles in inducing mitotic arrest, apoptosis, and mitotic cell death. However, its roles during oocyte meiotic maturation have not been fully defined. In this study, we report that Kif16A exhibits unique accumulation on the spindle apparatus and colocalizes with microtubule fibers during mouse oocyte meiotic maturation. Targeted depletion of Kif16A using gene‐targeting siRNA disrupts the progression of the meiotic cell cycle. Furthermore, Kif16A depletion leads to aberrant spindle assembly and chromosome misalignment in oocytes. Our findings also indicate that Kif16A depletion reduces tubulin acetylation levels and compromises microtubule resistance to depolymerizing drugs, suggesting its crucial role in microtubule stability maintenance. Notably, we find that the depletion of Kif16A results in a notably elevated incidence of defective kinetochore‐microtubule attachments and the absence of BubR1 localization at kinetochores, suggesting a critical role for Kif16A in the activation of the spindle assembly checkpoint (SAC) activity. Additionally, we observe that Kif16A is indispensable for proper actin filament distribution, thereby impacting spindle migration. In summary, our findings demonstrate that Kif16A plays a pivotal role in regulating microtubule and actin dynamics crucial for ensuring both spindle assembly and migration during mouse oocyte meiotic maturation.
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