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 ...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.展开更多
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)
文摘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.
