PUBLICATION
            Duplication and Diversification of the Hypoxia-Inducible IGFBP-1 Gene in Zebrafish
- Authors
- Kamei, H., Lu, L., Jiao, S., Li, Y., Gyrup, C., Laursen, L.S., Oxvig, C., Zhou, J., and Duan, C.
- ID
- ZDB-PUB-080908-9
- Date
- 2008
- Source
- PLoS One 3(8): e3091 (Journal)
- Registered Authors
- Duan, Cunming
- Keywords
- Zebrafish, Hypoxia, Embryos, Gene expression, Sequence motif analysis, Embryogenesis, Evolutionary genetics, Reverse transcriptase-polymerase chain reaction
- MeSH Terms
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                - Insulin-Like Growth Factor Binding Protein 1/classification
- Insulin-Like Growth Factor Binding Protein 1/genetics*
- Base Sequence
- Molecular Sequence Data
- Gene Expression Regulation
- Zebrafish/classification
- Zebrafish/genetics*
- Chromosome Mapping
- Phylogeny
- Gene Duplication*
- Sequence Alignment
- Animals
- Hypoxia/genetics
- Conserved Sequence
- Genetic Variation*
- Zebrafish Proteins/classification
- Zebrafish Proteins/genetics*
 
- PubMed
- 18769480 Full text @ PLoS One
            Citation
        
        
            Kamei, H., Lu, L., Jiao, S., Li, Y., Gyrup, C., Laursen, L.S., Oxvig, C., Zhou, J., and Duan, C. (2008) Duplication and Diversification of the Hypoxia-Inducible IGFBP-1 Gene in Zebrafish. PLoS One. 3(8):e3091.
        
    
                
                    
                        Abstract
                    
                    
                
                
            
        
        
    
        
            
            
 
    
    
        
    
    
    
        
                BACKGROUND: Gene duplication is the primary force of new gene evolution. Deciphering whether a pair of duplicated genes has evolved divergent functions is often challenging. The zebrafish is uniquely positioned to provide insight into the process of functional gene evolution due to its amenability to genetic and experimental manipulation and because it possess a large number of duplicated genes. METHODOLOGY/PRINCIPAL FINDINGS: We report the identification and characterization of two hypoxia-inducible genes in zebrafish that are co-ortholgs of human IGF binding protein-1 (IGFBP-1). IGFBP-1 is a secreted protein that binds to IGF and modulates IGF actions in somatic growth, development, and aging. Like their human and mouse counterparts, in adult zebrafish igfbp-1a and igfbp-1b are exclusively expressed in the liver. During embryogenesis, the two genes are expressed in overlapping spatial domains but with distinct temporal patterns. While zebrafish IGFBP-1a mRNA was easily detected throughout embryogenesis, IGFBP-1b mRNA was detectable only in advanced stages. Hypoxia induces igfbp-1a expression in early embryogenesis, but induces the igfbp-1b expression later in embryogenesis. Both IGFBP-1a and -b are capable of IGF binding, but IGFBP-1b has much lower affinities for IGF-I and -II because of greater dissociation rates. Overexpression of IGFBP-1a and -1b in zebrafish embryos caused significant decreases in growth and developmental rates. When tested in cultured zebrafish embryonic cells, IGFBP-1a and -1b both inhibited IGF-1-induced cell proliferation but the activity of IGFBP-1b was significantly weaker. CONCLUSIONS/SIGNIFICANCE: These results indicate subfunction partitioning of the duplicated IGFBP-1 genes at the levels of gene expression, physiological regulation, protein structure, and biological actions. The duplicated IGFBP-1 may provide additional flexibility in fine-tuning IGF signaling activities under hypoxia and other catabolic conditions.
            
    
        
        
    
    
    
                
                    
                        Genes / Markers
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Expression
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Phenotype
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Mutations / Transgenics
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Human Disease / Model
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Sequence Targeting Reagents
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Fish
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Orthology
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Engineered Foreign Genes
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Mapping
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    