PUBLICATION
            Gdf11 regulates left-right asymmetry development through TGF-β signal
- Authors
 - Yao, W., Wei, Z., Tian, X., Tan, J., Liu, J.
 - ID
 - ZDB-PUB-241016-12
 - Date
 - 2024
 - Source
 - Cell Proliferation : e13765e13765 (Journal)
 - Registered Authors
 - Liu, Jingwen
 - Keywords
 - none
 - MeSH Terms
 - 
    
        
        
            
                
- Transforming Growth Factor beta*/metabolism
 - Animals
 - Signal Transduction*
 - Zebrafish*/embryology
 - Zebrafish*/metabolism
 - Zebrafish Proteins*/genetics
 - Zebrafish Proteins*/metabolism
 - Smad2 Protein/metabolism
 - Gene Expression Regulation, Developmental
 - Forkhead Transcription Factors/genetics
 - Forkhead Transcription Factors/metabolism
 - Growth Differentiation Factors*/genetics
 - Growth Differentiation Factors*/metabolism
 - Bone Morphogenetic Proteins/metabolism
 - Body Patterning*/genetics
 
 - PubMed
 - 39407407 Full text @ Cell Prolif.
 
            Citation
        
        
            Yao, W., Wei, Z., Tian, X., Tan, J., Liu, J. (2024) Gdf11 regulates left-right asymmetry development through TGF-β signal. Cell Proliferation. :e13765e13765.
        
    
                
                    
                        Abstract
                    
                    
                
                
            
        
        
    
        
            
            
 
    
    
        
    
    
    
        
                During the embryonic developmental stage in vertebrates, internal organs are arranged along the left-right axis. Disruptions in this process can result in congenital diseases or laterality disorders. The molecular mechanisms of left-right asymmetry in vertebrate development remain largely unclear. Due to its straightforward structure, zebrafish has become a favoured model for studying early laterality events. Here, we demonstrate that growth and development factor 11 (Gdf11) is essential for left-right development via TGF-β signalling. Morphological analysis showed that gdf11 morphants and mutants displayed clear heart and liver laterality disorders in a Nodal signal-dependent manner. Additionally, we found that Kupffer's vesicle formation and ciliogenesis were impaired following gdf11 deletion. We also observed that Gdf11 may form a heterodimer with Spaw, which promotes Smad2/3 phosphorylation and activates TGF-β signalling. Subsequently, Gdf11 promotes left-right laterality by stimulating Foxj1a and its target gene expression. In summary, we reveal a critical role of Gdf11 in left-right patterning, providing fundamental insights into the developmental process of left-right asymmetry.
            
    
        
        
    
    
    
                
                    
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                        Fish
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Orthology
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
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