Fig. 1

Schematic diagram of gonadotropin-induced meiosis I (MI) resumption. During the female menstrual cycle, GnRH secreted by the hypothalamus promotes the release of LH and FSH from the anterior pituitary. The LH surge shuts down follicular GJs to prevent the entry of cAMP and cGMP from GCs into oocytes. FSH upregulates cAMP levels in GCs and stimulates cumulus expansion. LH inhibits the NPPC-NPR2 signaling pathway by activating the EGFR-Ca²⁺ signaling pathway to downregulate cGMP levels in GCs, thereby reducing cGMP levels in oocytes and activating PDE3A-mediated hydrolysis of cAMP. Low cAMP levels activate MPF, which consists of CDK1 and cyclin B1, thereby promoting oocyte MI resumption. MPF not only phosphorylates and inactivates protein phosphatase 1 (PP1) but also phosphorylates APC/C to help maintain phosphorylation of other CDK1 substrates. Phosphorylation of lamin A/C leads to nuclear membrane rupture, which in turn promotes oocyte MI resumption