ERK1/2 Activities Are Dispensable for Oocyte Growth but Are Required for Meiotic Maturation and Pronuclear Formation in Mouse

作     者：Yin-Li Zhang Xiao-Man Liu Shu-Yan Ji Qian-Qian Sha Jue Zhang Heng-Yu Fan 

作者机构：Life Sciences Institute Zhejiang University 

出 版 物：《Journal of Genetics and Genomics》 (遗传学报（英文版）)

年 卷 期：2015年第42卷第9期

页      面：477-485页

核心收录：

学科分类：0905[农学-畜牧学] 09[农学] 090501[农学-动物遗传育种与繁殖] 

基　　金：supported by the National Basic Research Program of China (Nos. 2011CB944504 and 2012CB944403) the National Natural Science Foundation of China (Nos. 81172473 and 31371449) 

主　　题：Oocyte Female reproduction Meiosis ERK1/2 Fertilization 

摘      要：Previous studies revealed that extracellular regulated kinase-1 and -2 （ERK1/2） cascade plays pivotal roles in regulating oocyte meiotic cell cycle progression. However, most knowledge about the in vivo function of ERK1/2 in mammalian oocytes was indirectly obtained from analyzing the phenotypes of Mos knockout mice. In this study, we knocked out Erkl and Erk2 in mouse oocytes as early as the primordial follicle stage using the well-characterized Gdp-Cre mouse model, and for the first time directly investigated the in vivo function of ERK1/2 in mouse oocytes. In this novel mouse model, we observed that ERK1/2 activities in oocyte are dispensable for primordial follicle maintenance, activation and follicle growth. Different from the Mos null oocytes, the ERK1/2-deleted oocytes had well-assembled spindles at metaphase I （MI）, extruded polar body-I （PB1） with normal sizes, and did not undergo a full parthenogenetic activation characterized for pronuclear formation. However, the ovulated ERK1/2-deleted oocytes had poorly-assembled metaphase II （MII） spindles, spontaneously released polar body-2 （PB2）, and were arrested at another metaphase called metaphase III （MIII）. In addition, ERK1/2 deletion prevented male pronuclear formation after fertilization, and caused female infertility. In conclusion, these results indicate that ERK1/2 activities are required for not only MII-arrest maintenance, but also efficient pronuclear formation in mouse oocytes.