Nucleic Acids Research, 1992, Vol. 20, No. 11 2877-2884
© 1992
MOLECULAR BIOLOGY |
Distinct activation of murine interferon-
promoter region by IRF-1/ISFG-2 and virus infection
1Oncology Center, The Johns Hopkins University School of Medicine Baltimore, Maryland 21205 2Department of Molecular Biology and Genetics, The Johns Hopkins University School of Medicine Baltimore, Maryland 21205 3Laboratory of Molecular Cell Biology, Rockefeller University New York, NY 10021, USA
* To whom correspondence should be addressed
Received December 4, 1991. Revised May 8, 1992. Accepted May 8, 1992.
Virus infection in mouse L929 cells activates expression of interferon-
4 (IFN-4), but not IFN-6. The integrity of a symmetrical sequence, GTAAAGAAA-GT (F1 site); (–103 to –93), present in the 35 nucleotide (nt) long inducible element (IE) (–109 to –75) of the 4 promoter region is essential for the virus-induced expression. In the present study, we have shown that the interferon regulatory factor 1 (IRF-1) can induce expression of both IFN-4 and -6 in a transient expression assay. Virus infection cooperates with IRF-1 and further enhances transcription from the 4 promoter, but inhibits the IRF-1-mediated expression from the 6 promoter. The virus-mediated induction is determined by both IRF-1 and F1 sites, while activation by IRF-1 in a cotransfection assay is not greatly influenced by the F1 sequence. The activation of IFN- gene promoters by IRF-1 was limited to the transient expression assay. The integrated 4 promoter or the endogenous IFN- genes could not be induced by transfection with IRF-1 expressing plasmid and IRF-1 did not up-regulate expression of the endogenous IRF-1 gene. However, expression of IRF-1 alone was sufficient to up-regulate the expression of two IFN stimulated genes, 2',5' oligoadenylate synthetase (OAS) and interferon stimulated (ISG)-15 gene. These results suggest that induction of IFN- gene expression by virus infection requires cooperation between IRF-1 and another factor(s) that binds to the F1 sequence.
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