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Molecular and Cellular Biology, July 2002, p. 4450-4462, Vol. 22, No. 13
0270-7306/02/$04.00+0     DOI: 10.1128/MCB.22.13.4450-4462.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Acetylation of Nucleosomal Histones by p300 Facilitates Transcription from Tax-Responsive Human T-Cell Leukemia Virus Type 1 Chromatin Template

Hanxin Lu,1,2 Cynthia A. Pise-Masison,1 Terace M. Fletcher,3 R. Louis Schiltz,4 Akhilesh K. Nagaich,3 Michael Radonovich,1 Gordon Hager,3 Philip A. Cole,5 and John N. Brady1*

Virus Tumor Biology Section, Basic Research Laboratory,1 Laboratory of Receptor Biology and Gene Expression, National Cancer Institute,3 Muscle Gene Expression Group, Laboratory of Muscle Biology, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland 20892,4 Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205,5 Graduate Genetics Program, Institute for Biomedical Sciences, The George Washington University, Washington, D.C. 200372

Received 7 December 2001/ Returned for modification 6 February 2002/ Accepted 9 April 2002

Expression of human T-cell leukemia virus type 1 (HTLV-1) is regulated by the viral transcriptional activator Tax. Tax activates viral transcription through interaction with the cellular transcription factor CREB and the coactivators CBP/p300. One key property of the coactivators is the presence of histone acetyltransferase (HAT) activity, which enables p300/CBP to modify nucleosome structure. The data presented in this manuscript demonstrate that full-length p300 and CBP facilitate transcription of a reconstituted chromatin template in the presence of Tax and CREB. The ability of p300 and CBP to activate transcription from the chromatin template is dependent upon the HAT activity. Moreover, the coactivator HAT activity must be tethered to the template by Tax and CREB, since a p300 mutant that fails to interact with Tax did not facilitate transcription or acetylate histones. p300 acetylates histones H3 and H4 within nucleosomes located in the promoter and 5' proximal regions of the template. Nucleosome acetylation is accompanied by an increase in the level of binding of RNA polymerase II transcription factor TFIID and RNA polymerase II to the promoter. Interestingly, we found distinct transcriptional activities between CBP and p300. CBP, but not p300, possesses an N-terminal activation domain which directly activates Tax-mediated HTLV-1 transcription from a naked DNA template. Finally, using the chromatin immunoprecipitation assay, we provide the first direct experimental evidence that p300 and CBP are associated with the HTLV-1 long terminal repeat in vivo.

* Corresponding author. Mailing address: Virus Tumor Biology Section, BRL, NCI, NIH, Bethesda, MD 20892. Phone: (301) 496-0986. Fax: (301) 496-4951. E-mail: bradyj{at}mail.nih.gov.

Molecular and Cellular Biology, July 2002, p. 4450-4462, Vol. 22, No. 13
0022-538X/02/$04.00+0     DOI: 10.1128/MCB.22.13.4450-4462.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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