CenpH regulates meiotic G2/M transition by modulating the APC/CCdh1-cyclin B1 pathway in oocytes

Abstract

Meiotic resumption (G2/M transition) and progression through meiosis I (MI) are two critical stages for producing fertilization-competent eggs. Here, we report that CenpH, a component of the kinetochore inner plate protein, is responsible for the G2/M transition in meiotic mouse oocytes. Depletion of CenpH using morpholino injection decreased cyclin B1 levels, resulting in an attenuation of MPF activation, and severely compromised the meiotic resumption. CenpH protects cyclin B1 from destruction by competing actions of APC/CCdh1. Impaired G2/M transition after CenpH depletion could be rescued by expression of exogenous cyclin B1. Unexpectedly, blocking of CenpH did not affect spindle organization and meiotic cell cycle progression after germinal vesicle breakdown. Our findings reveal a novel role of CenpH in regulating meiotic G2/M transition by acting via the APC/CCdh1-cyclin B1 pathway.