|ZFIN ID: ZDB-PUB-181228-6|
Loss-of-function of sox3 causes follicle development retardation and reduces fecundity in zebrafish
Hong, Q., Li, C., Ying, R., Lin, H., Li, J., Zhao, Y., Cheng, H., Zhou, R.
|Source:||Protein & cell 10(5): 347-364 (Journal)|
|Registered Authors:||Zhou, Rongjia|
|Keywords:||Cyp19a1a, Sox3, apoptosis, follicle development, zebrafish|
|PubMed:||30588557 Full text @ Protein Cell|
Hong, Q., Li, C., Ying, R., Lin, H., Li, J., Zhao, Y., Cheng, H., Zhou, R. (2018) Loss-of-function of sox3 causes follicle development retardation and reduces fecundity in zebrafish. Protein & cell. 10(5):347-364.
ABSTRACTFolliculogenesis 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.