PUBLICATION
            Zebrafish CiA interneurons are late-born primary neurons
- Authors
 - Yeo, S.Y.
 - ID
 - ZDB-PUB-091023-14
 - Date
 - 2009
 - Source
 - Neuroscience letters 466(3): 131-134 (Journal)
 - Registered Authors
 - Yeo, Sang-Yeob
 - Keywords
 - Notch, Zebrafish, Pax2, CiA, Primary neurons, Late-born neurons, Mind bomb, CoPA
 - MeSH Terms
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- Animals
 - Spinal Cord/cytology
 - Spinal Cord/embryology
 - Spinal Cord/metabolism
 - Xenopus
 - Embryo, Nonmammalian
 - Immunohistochemistry
 - Zebrafish/embryology*
 - Zebrafish/metabolism
 - Interneurons/cytology*
 - Interneurons/metabolism
 - Gene Knockdown Techniques
 - Ubiquitin-Protein Ligases/genetics
 - Receptors, Notch/genetics
 - Neurons/cytology*
 - Neurons/metabolism
 - Mutation
 - RNA, Messenger/genetics
 - Zebrafish Proteins/biosynthesis
 - Zebrafish Proteins/genetics
 - PAX2 Transcription Factor/biosynthesis
 
 - PubMed
 - 19800937 Full text @ Neurosci. Lett.
 
            Citation
        
        
            Yeo, S.Y. (2009) Zebrafish CiA interneurons are late-born primary neurons. Neuroscience letters. 466(3):131-134.
        
    
                
                    
                        Abstract
                    
                    
                
                
            
        
        
    
        
            
            
 
    
    
        
    
    
    
        
                Pax2 is a neural-related transcription factor downstream of Notch signaling and is expressed in the developing spinal cord of zebrafish, including in CiA interneurons. However, the characteristics of pax2-positive neurons are largely unknown. The goal of this study was to characterize Pax2-positive neurons by examining their expression in embryos in which Notch function had been knocked down by mutation or injection of a morpholino or mRNA. I found that Pax2-positive CiA interneurons were late-differentiating primary neurons. pax2.1 was expressed in CoPA commissural neurons and CiA interneurons at 26 hpf. The number of pax2.1-positive cells increased in mind bomb mutant embryos or embryos injected with Su(H)1-MO, but not in cells injected with Xenopus Delta or Delta(stu) mRNA. These observations imply that Notch signaling plays a role in regulating the number of CiA neurons by preventing uncommitted precursors from acquiring a neuronal fate during vertebrate development.
            
    
        
        
    
    
    
                
                    
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