Kinesin KIF16B Participates in G2/M Transition and Microtubule Dynamics via Aurora A-PLK1 in Oocyte Meiosis

Abstract

KIF16B is a member of the kinesin-3 family of motor proteins, which facilitates processes such as vesicle transport, microtubule dynamics, and organelle function during mitosis. In this study, we explored the role of KIF16B in meiosis. Our findings indicate that KIF16B is involved in the meiotic G2–M transition and spindle assembly in oocytes. KIF16B was consistently expressed throughout the meiotic cell cycle of mouse oocytes. After the occurrence of germinal vesicle breakdown, KIF16B became concentrated on microtubules. The exhaustion of KIF16B induced the impairment of meiotic cell cycle progression, which was due to the inactivation of CDK1 and the reduction in the level of cyclin B1, consequently resulting in the failure of germinal vesicle breakdown. Furthermore, aberrant spindle phenotypes and disordered chromosome alignment were observed in KIF16B-depleted oocytes, along with improper kinetochore–microtubule attachments. These abnormal K–MT attachments resulted in the persistent activation of BubR1/Bub3 at the kinetochores. Moreover, KIF16B knockdown destabilized α-tubulin by affecting the activity of histone deacetylase 6 (HDAC6). Further analysis revealed that KIF16B participated in the Ran GTPase-dependent activation of TPX2, which in turn regulated the phosphorylation levels of Aurora A–polo-like kinase 1 (PLK1), driving the proper assembly of the spindle. In conclusion, our data indicated that KIF16B is crucial for meiosis resumption and spindle assembly in mouse oocytes.