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Journal of Virology, June 2002, p. 5532-5539, Vol. 76, No. 11
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.11.5532-5539.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Transcriptional Profiling of Interferon Regulatory Factor 3 Target Genes: Direct Involvement in the Regulation of Interferon-Stimulated Genes

Nathalie Grandvaux,1,3 Marc J. Servant,1,3 Benjamin tenOever,1,3 Ganes C. Sen,4 Siddarth Balachandran,5 Glen N. Barber,5 Rongtuan Lin,1,3 and John Hiscott1,2,3*

Terry Fox Molecular Oncology Group, Lady Davis Institute for Medical Research,1 Departments of Microbiology and Immunology,2 Medicine, McGill University, Montreal, Quebec H3T 1E2, Canada,3 Department of Molecular Biology, Cleveland Clinic Foundation, Cleveland, Ohio 44195,4 Department of Microbiology and Immunology, University of Miami School of Medicine, Miami, Florida 331365

Received 17 December 2001/ Accepted 20 February 2002

Ubiquitously expressed interferon regulatory factor 3 (IRF-3) is directly activated after virus infection and functions as a key activator of the immediate-early alpha/beta interferon (IFN) genes, as well as the RANTES chemokine gene. In the present study, a tetracycline-inducible expression system expressing a constitutively active form of IRF-3 (IRF-3 5D) was combined with DNA microarray analysis to identify target genes regulated by IRF-3. Changes in mRNA expression profiles of 8,556 genes were monitored after Tet-inducible expression of IRF-3 5D. Among the genes upregulated by IRF-3 were transcripts for several known IFN-stimulated genes (ISGs). Subsequent analysis revealed that IRF-3 directly induced the expression of ISG56 in an IFN-independent manner through the IFN-stimulated responsive elements (ISREs) of the ISG56 promoter. These results demonstrate that, in addition to its role in the formation of a functional immediate-early IFN-ß enhanceosome, IRF-3 is able to discriminate among ISRE-containing genes involved in the establishment of the antiviral state as a direct response to virus infection.

* Corresponding author. Mailing address: Molecular Oncology Group, Lady Davis Institute for Medical Research, 3755 Chemin de la Cote Sainte Catherine, Montreal, Quebec H3T 1E2, Canada. Phone: (514) 340-8222, ext. 5265. Fax: (514) 340-7576. E-mail: john.hiscott{at}mcgill.ca.

Journal of Virology, June 2002, p. 5532-5539, Vol. 76, No. 11
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.11.5532-5539.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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