PUBLICATION
            Catch-up growth in zebrafish embryo requires neural crest cells sustained by Irs1-signaling
- Authors
- Kamei, H., Yoneyama, Y., Hakuno, F., Sawada, R., Shimizu, T., Duan, C., Takahashi, S.I.
- ID
- ZDB-PUB-180202-7
- Date
- 2018
- Source
- Endocrinology 159(4): 1547-1560 (Journal)
- Registered Authors
- Duan, Cunming
- Keywords
- none
- MeSH Terms
- 
    
        
        
            
                - Embryo, Nonmammalian/metabolism*
- Animals
- Zebrafish
- Multipotent Stem Cells/metabolism*
- Neural Crest/metabolism*
- Embryonic Development/physiology*
- Insulin Receptor Substrate Proteins/genetics
- Insulin Receptor Substrate Proteins/metabolism*
- Hypoxia/metabolism
- Signal Transduction/physiology*
- Proto-Oncogene Proteins c-akt/metabolism
 
- PubMed
- 29390112 Full text @ Endocrinology
            Citation
        
        
            Kamei, H., Yoneyama, Y., Hakuno, F., Sawada, R., Shimizu, T., Duan, C., Takahashi, S.I. (2018) Catch-up growth in zebrafish embryo requires neural crest cells sustained by Irs1-signaling. Endocrinology. 159(4):1547-1560.
        
    
                
                    
                        Abstract
                    
                    
                
                
            
        
        
    
        
            
            
 
    
    
        
    
    
    
        
                Most animals display retarded growth in adverse conditions; however, upon the removal of unfavorable factors, they often show quick growth restoration, which is known as "catch-up" growth. In zebrafish embryos, hypoxia causes growth arrest but subsequent reoxygenation induces the catch-up growth. Here we report the role of Irs1-mediated insulin/insulin-like growth factor signaling (IIS) and the involvement of stem cells in catch-up growth in reoxygenated zebrafish embryos. Disturbed irs1 expression attenuated IIS resulting in greater growth inhibition in catch-up growth than in normal growth, and forced IIS-activation restored the catch-up growth. The irs1 knockdown induced noticeable cell-death in neural crest cells (NCCs), multipotent stem cells, under hypoxia, and the pharmacological/genetic ablation of NCCs hindered the catch-up growth. Furthermore, inhibition of the apoptotic pathway by pan-Caspase inhibition or forced activation of Akt signaling in irs1 knocked-down embryos blocked NCC cell death and rescued catch-up growth. Our data indicate this multipotent stem cell is indispensable for the embryonic catch-up growth and the Irs1-mediated IIS is prerequisite for its survival under severe adverse environments such as prolonged hypoxia.
            
    
        
        
    
    
    
                
                    
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                        Fish
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Orthology
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
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