,Loss-of-function of sox3 causes follicle development retardation and reduces fecundity in zebrafish

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Folliculogenesis is essential for production of female gametes in vertebrates.However,the molecular mechanisms underlying follicle development,particularly apoptosis regulation in ovary,remain elusive.Here,we generated sox3 knockout zebrafish lines using CRISPR/Cas9.sox3 knockout led to follicle development retardation and a reduced fecundity in females.Comparative analysis of transcriptome between sox3-/-and wild-type ovaries revealed that Sox3 was involved in pathways of ovarian steroidogenesis and apoptosis.Knockout of sox3 promoted follicle apoptosis and obvious apoptosis signals were detected in somatic cells of stages Ⅲ and Ⅳ follicles of sox3-/-ovaries.Moreover,Sox3 can bind to and activate the promoter of cyp19a1a.Up-regulation of Cyp19a1a expression promoted 17β-estradiol synthesis,which inhibited apoptosis in follicle development.Thus,Sox3 functions as a regulator of Cyp19a1a expression,via 17β-E2 linking apoptosis suppression,which is implicated in improving female fecundity.
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