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Molecular and Cellular Biology, May 2004, p. 4476-4486, Vol. 24, No. 10
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.10.4476-4486.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

The Chromatin-Remodeling BAF Complex Mediates Cellular Antiviral Activities by Promoter Priming

Kairong Cui,1 Prafullakumar Tailor,2 Hong Liu,1 Xin Chen,3 Keiko Ozato,2 and Keji Zhao1*

Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute,1 Laboratory of Molecular Growth Regulation, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892,2 Department of Biopharmaceutical Sciences, University of California, San Francisco, California 941433

Received 26 September 2003/ Returned for modification 4 December 2003/ Accepted 11 February 2004

The elicitation of cellular antiviral activities is dependent on the rapid transcriptional activation of interferon (IFN) target genes. It is not clear how the interferon target promoters, which are organized into chromatin structures in cells, rapidly respond to interferon or viral stimulation. In this report, we show that alpha IFN (IFN-{alpha}) treatment of HeLa cells induced hundreds of genes. The induction of the majority of these genes was inhibited when one critical subunit of the chromatin-remodeling SWI/SNF-like BAF complexes, BAF47, was knocked down via RNA interference. Inhibition of BAF47 blocked the cellular response to viral infection and impaired cellular antiviral activity by inhibiting many IFN- and virus-inducible genes. We show that the BAF complex was required to mediate both the basal-level expression and the rapid induction of the antiviral genes. Further analyses indicated that the BAF complex primed some IFN target promoters by utilizing ATP-derived energy to maintain the chromatin in a constitutively open conformation, allowing faster and more potent induction after IFN-{alpha} treatment. We propose that constitutive binding of the BAF complex is an important mechanism for the IFN-inducible promoters to respond rapidly to IFN and virus stimulation.

* Corresponding author. Mailing address: 9000 Rockville Pike, Building 10, Room 7N311, Bethesda, MD 20892-1674. Phone: (301) 496-2098. Fax: (301) 480-0961. E-mail: zhaok{at}nhlbi.nih.gov.

Molecular and Cellular Biology, May 2004, p. 4476-4486, Vol. 24, No. 10
0022-538X/04/$08.00+0     DOI: 10.1128/MCB.24.10.4476-4486.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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