Investigating the molecular mechanisms of oocyte maturation and ovulation in Nile tilapia: A focus on the steroidogenic enzyme Cyp17a2.

Previous research has highlighted the significant role of progestins and glucocorticoids in fish oocyte maturation and ovulation. To clarify the molecular mechanisms underlying these processes, comprehensive investigations were conducted using a mutant Nile tilapia ( ) model. Analysis revealed pronounced Cyp17a2 expression in ovarian somatic cells of the tilapia. Female -deficient mutants exhibited markedly reduced levels of 17,20β-dihydroxy-4-pregnen-3-one (DHP) and cortisol/cortisone, leading to delayed meiotic initiation and impaired oocyte maturation and spawning. Notably, supplementation with human chorionic gonadotrophin (hCG), DHP, and cortisol effectively induced germinal vesicle breakdown (GVBD) and facilitated oocyte release with follicular cell layers in females. Additionally, and rescued females showed elevated transcription of steroidogenic enzymes involved in 17β-estradiol (E2) production compared to spawning wild-type females. Moreover, the reduction in Akt phosphorylation observed in -deficient females and upon inhibitor treatment impaired hCG-induced oocyte maturation. Conversely, activation of the phosphoinositide 3-kinase/protein kinase B (PI3K-Akt) signaling pathway partially rescued the oocyte maturation impairment caused by mutation. Overall, these findings provide functional evidence supporting the critical role of Cyp17a2 in DHP and cortisol biosynthesis, which, in turn, facilitates oocyte maturation and ovulation through activation of the PI3K-Akt signaling pathway in fish.