PUBLICATION
            Zebrafish Plzf transcription factors enhance early type I IFN response induced by two non-enveloped RNA viruses
- Authors
- Aleksejeva, E., Houel, A., Briolat, V., Levraud, J.P., Langevin, C., Boudinot, P.
- ID
- ZDB-PUB-160101-4
- Date
- 2016
- Source
- Developmental and comparative immunology 57: 48-56 (Journal)
- Registered Authors
- Briolat, Valerie, Levraud, Jean-Pierre
- Keywords
- PLZF, ZBTB, antiviral innate immunity, interferon, zebrafish
- MeSH Terms
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                - Poly I-C/immunology
- RNA, Viral/immunology
- Phylogeny
- RNA Viruses/immunology*
- Mice
- Zebrafish Proteins/classification
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- Interferon Type I/immunology*
- Interferon Type I/metabolism
- Animals
- Humans
- Immunity, Innate
- Kruppel-Like Transcription Factors/classification
- Kruppel-Like Transcription Factors/genetics
- Kruppel-Like Transcription Factors/metabolism*
- Zebrafish/genetics
- Zebrafish/immunology*
- RNA Virus Infections/immunology*
- Transcriptome
 
- PubMed
- 26719025 Full text @ Dev. Comp. Immunol.
            Citation
        
        
            Aleksejeva, E., Houel, A., Briolat, V., Levraud, J.P., Langevin, C., Boudinot, P. (2016) Zebrafish Plzf transcription factors enhance early type I IFN response induced by two non-enveloped RNA viruses. Developmental and comparative immunology. 57:48-56.
        
    
                
                    
                        Abstract
                    
                    
                
                
            
        
        
    
        
            
            
 
    
    
        
    
    
    
        
                The BTB-POZ transcription factor Promyelocytic Leukemia Zinc Finger (PLZF, or ZBTB16) has been recently identified as a major factor regulating the induction of a subset of Interferon stimulated genes in human and mouse. We show that the two co-orthologues of PLZF found in zebrafish show distinct expression patterns, especially in larvae. Although zbtb16a/plzfa and zbtb16b/plzfb are not modulated by IFN produced during viral infection, their over-expression increases the level of the early type I IFN response, at a critical phase in the race between the virus and the host response. The effect of Plzfb on IFN induction was also detectable after cell infection by different non-enveloped RNA viruses, but not after infection by the rhabdovirus SVCV. Our findings indicate that plzf implication in the regulation of type I IFN responses is conserved across vertebrates, but at multiple levels of the pathway and through different mechanisms.
            
    
        
        
    
    
    
                
                    
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                        Expression
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
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                        Human Disease / Model
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Sequence Targeting Reagents
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Fish
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Orthology
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Engineered Foreign Genes
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Mapping
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    