PUBLICATION
            Beta-arrestin1 regulates zebrafish hematopoiesis through binding to YY1 and relieving polycomb group repression
- Authors
 - Yue, R., Kang, J., Zhao, C., Hu, W., Tang, Y., Liu, X., and Pei, G.
 - ID
 - ZDB-PUB-091120-6
 - Date
 - 2009
 - Source
 - Cell 139(3): 535-546 (Journal)
 - Registered Authors
 - Keywords
 - DEVBIO, DNA, PROTEINS
 - Datasets
 - GEO:GSE17773
 - MeSH Terms
 - 
    
        
        
            
                
- Animals
 - Arrestins/metabolism*
 - Hematopoiesis*
 - Zebrafish Proteins/genetics
 - Zebrafish Proteins/metabolism*
 - Polycomb-Group Proteins
 - Repressor Proteins/metabolism*
 - Genes, Homeobox
 - Homeodomain Proteins/metabolism
 - Signal Transduction*
 - Zebrafish/genetics
 - Zebrafish/growth & development*
 - Zebrafish/metabolism*
 - YY1 Transcription Factor/metabolism*
 
 - PubMed
 - 19879840 Full text @ Cell
 
            Citation
        
        
            Yue, R., Kang, J., Zhao, C., Hu, W., Tang, Y., Liu, X., and Pei, G. (2009) Beta-arrestin1 regulates zebrafish hematopoiesis through binding to YY1 and relieving polycomb group repression. Cell. 139(3):535-546.
        
    
                
                    
                        Abstract
                    
                    
                
                
            
        
        
    
        
            
            
 
    
    
        
    
    
    
        
                Beta-arrestin1 is a multifunctional protein critically involved in signal transduction. Recently, it is also identified as a nuclear transcriptional regulator, but the underlying mechanisms and physiological significance remain to be explored. Here, we identified beta-arrestin1 as an evolutionarily conserved protein essential for zebrafish development. Zebrafish embryos depleted of beta-arrestin1 displayed severe posterior defects and especially failed to undergo hematopoiesis. In addition, the expression of cdx4, a critical regulator of embryonic blood formation, and its downstream hox genes were downregulated by depletion of beta-arrestin1, while injection of cdx4, hoxa9a or hoxb4a mRNA rescued the hematopoietic defects. Further mechanistic studies revealed that beta-arrestin1 bound to and sequestered the polycomb group (PcG) recruiter YY1, and relieved PcG-mediated repression of cdx4-hox pathway, thus regulating hematopoietic lineage specification. Taken together, this study demonstrated a critical role of beta-arrestin1 during zebrafish primitive hematopoiesis, as well as an important regulator of PcG proteins and cdx4-hox pathway.
            
    
        
        
    
    
    
                
                    
                        Genes / Markers
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Expression
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
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                        Mutations / Transgenics
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Human Disease / Model
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Sequence Targeting Reagents
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Fish
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Orthology
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Engineered Foreign Genes
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Mapping