PUBLICATION
            Jagged 2b induces intercellular signaling within somites to establish hematopoietic stem cell fate in zebrafish
- Authors
 - Wada, Y., Tsukatani, H., Kuroda, C., Miyazaki, Y., Otoshi, M., Kobayashi, I.
 - ID
 - ZDB-PUB-220408-7
 - Date
 - 2022
 - Source
 - Development (Cambridge, England) 149(7): (Journal)
 - Registered Authors
 - Kobayashi, Isao
 - Keywords
 - Ephrin, Hematopoietic stem cells, Jagged, Notch, Somite, Zebrafish
 - MeSH Terms
 - 
    
        
        
            
                
- Signal Transduction
 - Hematopoietic Stem Cells/metabolism
 - Wnt Proteins/metabolism
 - Gene Expression Regulation, Developmental
 - Receptors, Notch/metabolism
 - Somites*/metabolism
 - Animals
 - Zebrafish*/genetics
 - Zebrafish*/metabolism
 - Zebrafish Proteins/genetics
 - Zebrafish Proteins/metabolism
 
 - PubMed
 - 35388409 Full text @ Development
 
            Citation
        
        
            Wada, Y., Tsukatani, H., Kuroda, C., Miyazaki, Y., Otoshi, M., Kobayashi, I. (2022) Jagged 2b induces intercellular signaling within somites to establish hematopoietic stem cell fate in zebrafish. Development (Cambridge, England). 149(7).
        
    
                
                    
                        Abstract
                    
                    
                
                
            
        
        
    
        
            
            
 
    
    
        
    
    
    
        
                During development, the somites play a key role in the specification of hematopoietic stem cells (HSCs). In zebrafish, the somitic Notch ligands Delta-c (Dlc) and Dld, both of which are regulated by Wnt16, directly instruct HSC fate in a shared vascular precursor. However, it remains unclear how this signaling cascade is spatially and temporally regulated within somites. Here, we show in zebrafish that an additional somitic Notch ligand, Jagged 2b (Jag2b), induces intercellular signaling to drive wnt16 expression. Jag2b activated Notch signaling in segmented somites at the early stage of somitogenesis. Loss of jag2b led to a reduction in the expression of wnt16 in the somites and an HSC marker, runx1, in the dorsal aorta, whereas overexpression of jag2b increased both. However, Notch-activated cells were adjacent to, but did not overlap with, wnt16-expressing cells within the somites, suggesting that an additional signaling molecule mediates this intercellular signal transduction. We uncover that Jag2b-driven Notch signaling induces efna1b expression, which regulates wnt16 expression in neighboring somitic cells. Collectively, we provide evidence for previously unidentified spatiotemporal regulatory mechanisms of HSC specification by somites.
            
    
        
        
    
    
    
                
                    
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