PUBLICATION
            A Rap GTPase interactor, RADIL, mediates migration of neural crest precursors
- Authors
 - Smolen, G.A., Schott, B.J., Stewart, R.A., Diederichs, S., Muir, B., Provencher, H.L., Look, A.T., Sgroi, D.C., Peterson, R.T., and Haber, D.A.
 - ID
 - ZDB-PUB-070827-2
 - Date
 - 2007
 - Source
 - Genes & Development 21(17): 2131-2136 (Journal)
 - Registered Authors
 - Look, A. Thomas, Peterson, Randall, Stewart, Rodney A.
 - Keywords
 - Neural crest, migration, adhesion, Rap, development, zebrafish
 - MeSH Terms
 - 
    
        
        
            
                
- Animals
 - Genes, ras
 - Gene Expression Regulation, Developmental
 - Zebrafish Proteins/physiology*
 - Cell Movement/genetics*
 - Morphogenesis/genetics*
 - Neural Crest/embryology*
 - Animals, Genetically Modified
 - Embryo, Nonmammalian
 - Carrier Proteins/physiology*
 - Cell Adhesion/genetics*
 - Genes, vpr*
 - rap GTP-Binding Proteins/physiology*
 
 - PubMed
 - 17704304 Full text @ Genes & Dev.
 
            Citation
        
        
            Smolen, G.A., Schott, B.J., Stewart, R.A., Diederichs, S., Muir, B., Provencher, H.L., Look, A.T., Sgroi, D.C., Peterson, R.T., and Haber, D.A. (2007) A Rap GTPase interactor, RADIL, mediates migration of neural crest precursors. Genes & Development. 21(17):2131-2136.
        
    
                
                    
                        Abstract
                    
                    
                
                
            
        
        
    
        
            
            
 
    
    
        
    
    
    
        
                The neural crest (NC) is a highly motile cell population that gives rise to multiple tissue lineages during vertebrate embryogenesis. Here, we identify a novel effector of the small GTPase Rap, called RADIL (RA [Ras association] and DIL domains), and show that it is required for cell adhesion and migration. Knockdown of radil in the zebrafish model results in multiple defects in NC-derived lineages such as cartilage, pigment cells, and enteric neurons. We specifically show that these defects are primarily due to the diminished migratory capacity of NC cells. The identification of RADIL as a regulator of NC migration defines a role for the Rap pathway in this process.
            
    
        
        
    
    
    
                
                    
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