Loss-of-function of sox3 causes follicle development retardation and reduces fecundity in zebrafish.
10.1007/s13238-018-0603-y
- Author:
Qiang HONG
1
;
Cong LI
1
;
Ruhong YING
1
;
Heming LIN
1
;
Jingqiu LI
1
;
Yu ZHAO
1
;
Hanhua CHENG
2
;
Rongjia ZHOU
3
Author Information
1. Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan, 430072, China.
2. Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan, 430072, China. hhcheng@whu.edu.cn.
3. Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan, 430072, China. rjzhou@whu.edu.cn.
- Publication Type:Journal Article
- Keywords:
Cyp19a1a;
Sox3;
apoptosis;
follicle development;
zebrafish
- From:
Protein & Cell
2019;10(5):347-364
- CountryChina
- Language:English
-
Abstract:
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.
