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

被引：12

作者：

Zhang, Teng ^{[1
,2
]}

Zhou, Yang ^{[1
,3
]}

Li, Li ^{[1
,4
]}

Wang, Zhen-Bo ^{[1
]}

Shen, Wei

Schatten, Heide ^{[5
]}

Sun, Qing-Yuan ^{[1
,2
,3
]}

机构：

[1] Chinese Acad Sci, Inst Zool, State Key Lab Stem Cell & Reprod Biol, Beijing 100101, Peoples R China

[2] Qingdao Agr Univ, Coll Anim Sci & Technol, Inst Reprod Sci, Qingdao 266109, Peoples R China

[3] Univ Chinese Acad Sci, Beijing 100049, Peoples R China

[4] Guangdong Women & Children Hosp, Dept Reprod Med, Guangzhou 510010, Guangdong, Peoples R China

[5] Univ Missouri, Dept Vet Pathobiol, Columbia, MO 65211 USA

来源：

DEVELOPMENT | 2017年 / 144卷 / 02期

基金：

中国国家自然科学基金;

关键词：

CenpH; G2/M transition; Cyclin B1; APC/C-Cdh1; Fzr1; Meiosis; Oocyte; PROPHASE-I ARREST; MOUSE OOCYTES; M-PHASE; KINETOCHORE PROTEIN; VERTEBRATE CELLS; CHECKPOINT; RESUMPTION; MATURATION; COMPLEX; PROMETAPHASE;

D O I：

10.1242/dev.141135

中图分类号：

Q [生物科学];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Meiotic resumption (G2/M transition) and progression through meiosis I (MI) are two key stages for producing fertilization-competent eggs. Here, we report that CenpH, a component of the kinetochore inner plate, is responsible for G2/M transition in meiotic mouse oocytes. Depletion of CenpH by morpholino injection decreased cyclin B1 levels, resulting in attenuation of maturation-promoting factor (MPF) activation, and severely compromised meiotic resumption. CenpH protects cyclin B1 from destruction by competing with the action of APC/C-Cdh1. Impaired G2/M transition after CenpH depletion could be rescued by expression of exogenous cyclin B1. Unexpectedly, blocking 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/C-Cdh1-cyclin B1 pathway.

引用

页码：305 / 312

页数：8

共 30 条

[1] Cdk1, but not Cdk2, is the sole Cdk that is essential and sufficient to drive resumption of meiosis in mouse oocytes [J].