FIGURE
            Fig. 3
- ID
- ZDB-FIG-100304-14
- Publication
- Wan et al., 2010 - Negative Feedback Regulation of Wnt4 Signaling by EAF1 and EAF2/U19
- Other Figures
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                        Fig. 3
                    
                    
                
                
            
        
        
    
        
            
            
| The knockdown of zebrafish Eaf1 and Eaf2/U19 rescues the embryonic defects caused by wnt4a over-expression. (A) Zebrafish embryos were co-injected with wnt4a mRNA (10 pg) and standard morpholino (STD) (8 ng). Defects, indicated by red arrows, included (b) folking notochord, (c) cyclopia, and (d) shortened axis. (B) (a) The embryos were co-injected with wnt4a mRNA and Eaf1/2-MO1to rescue the phenotype resembles wild-type embryos. (b) An example of a rescued embryo. (c) The efficiency of the Eaf1/Eaf2-MO1-mediated rescue is statistically significant (p<0.05) by counting defective embryos. | 
                
                    
                        Expression Data
                    
                    
                
                
            
        
        
    
        
            
            
            
            
    
    
                
                    
                        Expression Detail
                    
                    
                
                
            
        
        
    
        
            
                
            
        
    
    
    
                
                    
                        Antibody Labeling
                    
                    
                
                
            
        
        
    
        
            
                
            
        
    
    
    
                
                    
                        Phenotype Data
                    
                    
                
                
            
        
        
    
        
            
            
            
            
    
    
                
                    
                        Phenotype Detail
                    
                    
                
                
            
        
        
    
        
            
                
            
        
    
    
    
                
                    
                        Acknowledgments
                    
                    
                
                
            
        
        
    
        
            
            
                
                    
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      Full text @ PLoS One
                
                
            
        
        
    
    
     
        