The beta-interferon promoter responds to priming through multiple independent regulatory elements.
The induction of beta-interferon is markedly enhanced in some cell types by a pretreatment with type I interferon itself (priming). We show that induction in response to double-stranded RNA is completely dependent upon priming in HeLa cells. However, unprimed cells can be partially induced by Sendai virus. This indicates that Sendai virus can provide a signal that is different from, or additional to, that provided by double-stranded RNA. The requirement for priming cannot be localized to a specific sequence element in the beta-interferon promoter, suggesting that priming may induce an essential component for signal transduction in response to double-stranded RNA.
King
P
P
Gene Expression Laboratory, Imperial Cancer Research Fund, London, United Kingdom.
Goodbourn
S
S
D001483:Base Sequence; D015870:Gene Expression; D006367:HeLa Cells; D006801:Humans; D016899:Interferon-beta / Q000096:biosynthesis* / Q000235:genetics*; D007700:Kinetics; D008969:Molecular Sequence Data; D010222:Parainfluenza Virus 1, Human / Q000235:genetics; D010957:Plasmids; D011401:Promoter Regions, Genetic; D012330:RNA, Double-Stranded / Q000378:metabolism; D012045:Regulatory Sequences, Nucleic Acid; D017384:Sequence Deletion; D015398:Signal Transduction; D013539:Simian virus 40 / Q000235:genetics; D016385:TATA Box; D015533:Transcriptional Activation; D014162:Transfection
D012330:RNA, Double-Stranded; D016899:Interferon-beta