PUBLICATION
            Hedgehog and retinoic acid signaling cooperate to promote motoneurogenesis in zebrafish
- Authors
- Mich, J.K., and Chen, J.K.
- ID
- ZDB-PUB-111117-41
- Date
- 2011
- Source
- Development (Cambridge, England) 138(23): 5113-5119 (Journal)
- Registered Authors
- Chen, James K., Mich, John
- Keywords
- hedgehog, motoneuron, retinoic acid, zebrafish
- MeSH Terms
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                - Trans-Activators/metabolism
- Tretinoin/metabolism*
- Real-Time Polymerase Chain Reaction
- Zebrafish/physiology*
- In Situ Hybridization
- Motor Neurons/physiology*
- Neurogenesis/genetics
- Neurogenesis/physiology*
- Signal Transduction/physiology*
- Receptors, G-Protein-Coupled/deficiency*
- Oligonucleotides/genetics
- Zebrafish Proteins/deficiency*
- Oncogene Proteins/metabolism
- Hedgehog Proteins/metabolism*
- DNA Primers/genetics
- Animals
 
- PubMed
- 22069185 Full text @ Development
            Citation
        
        
            Mich, J.K., and Chen, J.K. (2011) Hedgehog and retinoic acid signaling cooperate to promote motoneurogenesis in zebrafish. Development (Cambridge, England). 138(23):5113-5119.
        
    
                
                    
                        Abstract
                    
                    
                
                
            
        
        
    
        
            
            
 
    
    
        
    
    
    
        
                The precise requirements of Hedgehog (Hh) pathway activity in vertebrate central nervous system development remain unclear,
                     particularly in organisms with both maternally and zygotically derived signaling. Here we describe the motoneural phenotype
                     of zebrafish that lack maternal and zygotic contributions of the Hh signaling transducer Smoothened (MZsmo mutants) and therefore are completely devoid of ligand-dependent pathway activation. Some functional primary motoneurons
                     (PMNs) persist in the absence of Hh signaling, and we find that their induction requires both basal Gli transcription factor
                     activity and retinoic acid (RA) signaling. We also provide evidence that RA pathway activation can modulate Gli function in
                     a Hh ligand-independent manner. These findings support a model in which Hh and RA signaling cooperate to promote PMN cell
                     fates in zebrafish.
            
    
        
        
    
    
    
                
                    
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                        Human Disease / Model
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Sequence Targeting Reagents
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Fish
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Orthology
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Engineered Foreign Genes
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Mapping
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    