FIGURE
            Fig. 7
- ID
- ZDB-FIG-110112-6
- Publication
- Robert-Moreno et al., 2010 - Characterization of new otic enhancers of the pou3f4 gene reveal distinct signaling pathway regulation and spatio-temporal patterns
- Other Figures
- All Figure Page
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                        Fig. 7
                    
                    
                
                
            
        
        
    
        
            
            
| Pax2 and Sox2 proteins are required for HCNR 81675 enhancer activation. (A) Scheme showing wild-type Sox and Pax2/5/8 consensus in the pou3f4 HCNR 81675 sequence and above each one, the mutation in the primers designed for site-directed mutagenesis of the Sox and Pax2/5/8 binding sites. (B–C) Transgenic embryos carrying GFP under the control of the HCNR 81675 enhancer. (B) GFP expression promoted by the wild type HCNR 81675 sequence. (C) GFP expression promoted by the HCNR 81675 enhancer harbouring the double mutation for Pax2/5/8 and Sox binding sites. | 
                
                    
                        Expression Data
                    
                    
                
                
            
        
        
    
        
            
            
            
            
    
    
                
                    
                        Expression Detail
                    
                    
                
                
            
        
        
    
        
            
                
            
        
    
    
    
                
                    
                        Antibody Labeling
                    
                    
                
                
            
        
        
    
        
            
                
            
        
    
    
    
                
                    
                        Phenotype Data
                    
                    
                
                
            
        
        
    
        
            
            
            
            
    
    
                
                    
                        Phenotype Detail
                    
                    
                
                
            
        
        
    
        
            
                
            
        
    
    
    
                
                    
                        Acknowledgments
                    
                    
                
                
            
        
        
    
        
            
            
                
                    
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      Full text @ PLoS One
                
                
            
        
        
    
    
     
        