PUBLICATION
            Genetic evidence for involvement of maternally derived Wnt canonical signaling in dorsal determination in zebrafish
- Authors
- Nojima, H., Shimizu, T., Kim, C.H., Yabe, T., Bae, Y.K., Muraoka, O., Hirata, T., Chitnis, A., Hirano, T., and Hibi, M.
- ID
- ZDB-PUB-040429-6
- Date
- 2004
- Source
- Mechanisms of Development 121(4): 371-386 (Journal)
- Registered Authors
- Bae, Young Ki, Chitnis, Ajay, Hibi, Masahiko, Hirata, Tsutomu, Kim, Cheol-Hee, Muraoka, Osamu, Nojima, Hideaki, Shimizu, Takashi, Yabe, Taijirou
- Keywords
- Maternal-effect mutant, Zebrafish, Wnt signaling, Organizer
- MeSH Terms
- 
    
        
        
            
                - Crosses, Genetic
- Zebrafish Proteins
- Body Patterning/genetics*
- Body Patterning/physiology
- Wnt Proteins
- Ligands
- Trans-Activators/metabolism
- Chromosome Mapping
- Cytoskeletal Proteins/metabolism
- Organizers, Embryonic/physiology
- Cell Nucleus/metabolism
- Signal Transduction/genetics*
- Signal Transduction/physiology
- Calcium Signaling/physiology
- Animals
- Proto-Oncogene Proteins/genetics*
- Proto-Oncogene Proteins/metabolism
- Zebrafish/embryology*
- Zebrafish/genetics
- Zebrafish/metabolism
- beta Catenin
 
- PubMed
- 15110047 Full text @ Mech. Dev.
            Citation
        
        
            Nojima, H., Shimizu, T., Kim, C.H., Yabe, T., Bae, Y.K., Muraoka, O., Hirata, T., Chitnis, A., Hirano, T., and Hibi, M. (2004) Genetic evidence for involvement of maternally derived Wnt canonical signaling in dorsal determination in zebrafish. Mechanisms of Development. 121(4):371-386.
        
    
                
                    
                        Abstract
                    
                    
                
                
            
        
        
    
        
            
            
 
    
    
        
    
    
    
        
                In zebrafish, the program for dorsal specification begins soon after fertilization. Dorsal determinants are localized initially to the vegetal pole, then transported to the blastoderm, where they are thought to activate the canonical Wnt pathway, which induces the expression of dorsal-specific genes. We identified a novel maternal-effect recessive mutation, tokkaebi (tkk), that affects formation of the dorsal axis. Severely ventralized phenotypes, including a lack of dorso-anterior structures, were seen in 5-100% of the embryos obtained from tkk homozygous transmitting females. tkk embryos displayed defects in the nuclear accumulation of beta-catenin on the dorsal side, and reduced or absent expression of dorsal-specific genes. Mesoderm and endoderm formation outside the dorsal axis was not significantly affected. Injection of RNAs for activated beta-catenin, dominant-negative forms of Axin1 and GSK3beta, and wild-type Dvl3, into the tkk embryos suppressed the ventralized phenotypes and/or dorsalized the embryos, and restored or induced an ectopic and expanded expression of bozozok/dharma and goosecoid. However, dorsalization by wnt RNAs was affected in the tkk embryos. Inhibition of cytoplasmic calcium release elicited an ectopic and expanded expression of chordin in the wild-type, but did not restore chordin expression efficiently in the tkk embryos. These data indicate that the tkk gene product functions upstream of or parallel to the beta-catenin-degradation machinery to control the stability of beta-catenin. The tkk locus was mapped to chromosome 16. These data provide genetic evidence that the maternally derived canonical Wnt pathway upstream of beta-catenin is involved in dorsal axis formation in zebrafish.
            
    
        
        
    
    
    
                
                    
                        Genes / Markers
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Expression
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Phenotype
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Mutations / Transgenics
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Human Disease / Model
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Sequence Targeting Reagents
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Fish
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Orthology
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Engineered Foreign Genes
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Mapping
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    