Infertility caused by retardation of follicular development in mice with oocyte-specific expression of Foxo3a

摘要: In recent years, mammalian oocytes have been proposed to important roles in the orchestration of ovarian follicular development and fertility. To determine whether intra-oocyte Foxo3a, a component phosphatidylinositol 3-kinase (PI3K) signaling pathway, influences female fertility, transgenic mouse model was generated with constitutively active Foxo3a expressed oocytes. We found that mice were infertile, which caused by retarded oocyte growth development, anovulation. Further mechanistic studies revealed dramatic reduction expression bone morphogenic protein 15 (Bmp15), connexin 37 43, are molecules for establishment paracrine gap junction communications follicles. also facilitate nuclear localization p27(kip1) oocytes, cyclin-dependent kinase (Cdk) inhibitor may serve inhibit growth. The results from current study indicate is an molecule negatively regulates development. Our therefore give some insight into oocyte-borne genetic aberrations cause defects anovulation human diseases, such as premature failure.