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Journal of Virology, October 2000, p. 8893-8903, Vol. 74, No. 19
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Promoter-Specific Targeting of Human SWI-SNF Complex by Epstein-Barr Virus Nuclear Protein 2

Daniel Y. Wu,1,2 Anton Krumm,3 and William H. Schubach1,2,*

Division of Medical Oncology, Department of Medicine, Veterans Administration Puget Sound Health Care System, Seattle Division, Seattle, Washington 98108,1 and Division of Medical Oncology, Department of Medicine, University of Washington Medical Center,2 and Division of Radiation Oncology, University of Washington,3 Seattle, Washington 98195

Received 26 April 2000/Accepted 7 July 2000

The multiprotein human SWI-SNF (hSWI-SNF) complex is a chromatin-remodeling machine that facilitates transcription by overcoming chromatin-mediated gene repression. We had previously shown that hSNF5/INI1, an intrinsic, consistent component of the hSWI/SNF complex, is associated with Epstein-Barr nuclear antigen 2 (EBNA2) and have proposed that EBNA2 directs this complex to key EBNA2-responsive viral and cellular genes. Using chromatin immunoprecipitation and quantitative PCR, we show that antibodies directed against components of the hSWI-SNF complex preferentially precipitate chromatin-associated DNA that contains a targeted EBNA2-responsive element in the context of both episomal and cellular chromatin. This enrichment does not occur in EBNA2-negative cells or when the EBNA2-responsive element is mutated. The stable association of the hSWI-SNF complex with the EBNA2-responsive promoter can also be disrupted by deletion of the TATA element, suggesting that EBNA2 in itself is insufficient to mediate stable targeting of the hSWI-SNF complex. These results demonstrate that recruitment of the hSWI-SNF complex to selected promoters can occur in vivo through its interaction with site-specific activator proteins and that stable targeting may require the presence of basal transcription factors.

* Corresponding author. Mailing address: 111-ONC, Division of Oncology, Veterans Administration Puget Sound Health Care System, Seattle Division, 1660 S. Columbian Way, Seattle, WA 98108. Phone: (206) 764-2709. Fax: (206) 764-2598. E-mail: wschu{at}u.washington.edu.

Journal of Virology, October 2000, p. 8893-8903, Vol. 74, No. 19
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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