PUBLICATION
            Loss of growth differentiation factor 9 causes an arrest of early folliculogenesis in zebrafish-A novel insight into its action mechanism
- Authors
 - Chen, W., Zhai, Y., Zhu, B., Wu, K., Fan, Y., Zhou, X., Liu, L., Ge, W.
 - ID
 - ZDB-PUB-221216-26
 - Date
 - 2022
 - Source
 - PLoS Genetics 18: e1010318e1010318 (Journal)
 - Registered Authors
 - Chen, Weiting, Fan, Yuqin, Ge, Wei, Zhu, Bo
 - Keywords
 - none
 - MeSH Terms
 - 
    
        
        
            
                
- Ovarian Follicle/metabolism
 - Animals
 - Growth Differentiation Factor 9*/genetics
 - Growth Differentiation Factor 9*/metabolism
 - Male
 - Mice
 - Female
 - Inhibins/genetics
 - Inhibins/metabolism
 - Zebrafish*/genetics
 - Zebrafish*/metabolism
 - Activins/genetics
 - Activins/metabolism
 
 - PubMed
 - 36520929 Full text @ PLoS Genet.
 
            Citation
        
        
            Chen, W., Zhai, Y., Zhu, B., Wu, K., Fan, Y., Zhou, X., Liu, L., Ge, W. (2022) Loss of growth differentiation factor 9 causes an arrest of early folliculogenesis in zebrafish-A novel insight into its action mechanism. PLoS Genetics. 18:e1010318e1010318.
        
    
                
                    
                        Abstract
                    
                    
                
                
            
        
        
    
        
            
            
 
    
    
        
    
    
    
        
                Growth differentiation factor 9 (GDF9) was the first oocyte-specific growth factor identified; however, most information about GDF9 functions comes from studies in the mouse model. In this study, we created a mutant for Gdf9 gene (gdf9-/-) in zebrafish using TALEN approach. The loss of Gdf9 caused a complete arrest of follicle development at primary growth (PG) stage. These follicles eventually degenerated, and all mutant females gradually changed to males through sex reversal, which could be prevented by mutation of the male-promoting gene dmrt1. Interestingly, the phenotypes of gdf9-/- could be rescued by simultaneous mutation of inhibin α (inha-/-) but not estradiol treatment, suggesting a potential role for the activin-inhibin system or its signaling pathway in Gdf9 actions. In gdf9 null follicles, the expression of activin βAa (inhbaa), but not βAb (inhbab) and βB (inhbb), decreased dramatically; however, its expression rebounded in the double mutant (gdf9-/-;inha-/-). These results indicate clearly that the activation of PG follicles to enter the secondary growth (SG) requires intrinsic factors from the oocyte, such as Gdf9, which in turn works on the neighboring follicle cells to trigger follicle activation, probably involving activins. In addition, our data also support the view that estrogens are not involved in follicle activation as recently reported.
            
    
        
        
    
    
    
                
                    
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                        Expression
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Phenotype
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Mutations / Transgenics
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Human Disease / Model
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Sequence Targeting Reagents
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Fish
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Orthology
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Engineered Foreign Genes
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Mapping