FIGURE
            Fig. 6
- ID
- ZDB-FIG-150202-16
- Publication
- Verleyen et al., 2014 - Orphan G-Protein Coupled Receptor 22 (Gpr22) Regulates Cilia Length and Structure in the Zebrafish Kupffer's Vesicle
- Other Figures
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                        Fig. 6
                    
                    
                
                
            
        
        
    
        
            
            
| 
 Gpr22 does not act upstream of Foxj1a/Rfx2 in KV ciliogenesis. (A, B) WISH of (A) foxj1a or (B) rfx2 on embryos at bud stage. Shown are (A) the lateral view with anterior to the left or (B) dorsal view with anterior to the top. gpr22 knock down or overexpression does not alter the DFC expression of foxj1a or rfx2, two master regulators of ciliogenesis. (C) Confirmation by qPCR of the foxj1a, rfx2 and polaris (target gene) RNA levels in the whole embryo, normalized to beta-actin. MO = morpholino, WISH = whole-mount in situ hybridization, DFC = dorsal forerunner cell, KV = Kupffer’s vesicle. | 
                
                    
                        Expression Data
                    
                    
                
                
            
        
        
    
        
            
            
    | Genes: | |
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| Fish: | |
| Knockdown Reagents: | |
| Anatomical Term: | |
| Stage: | Bud | 
                
                    
                        Expression Detail
                    
                    
                
                
            
        
        
    
        
            
                
            
        
    
    
    
                
                    
                        Antibody Labeling
                    
                    
                
                
            
        
        
    
        
            
                
            
        
    
    
    
                
                    
                        Phenotype Data
                    
                    
                
                
            
        
        
    
        
            
            
            
            
    
    
                
                    
                        Phenotype Detail
                    
                    
                
                
            
        
        
    
        
            
                
            
        
    
    
    
                
                    
                        Acknowledgments
                    
                    
                
                
            
        
        
    
        
            
            
                
                    
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      Full text @ PLoS One
                
                
            
        
        
    
    
     
        