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Journal of Virology, November 2006, p. 10542-10553, Vol. 80, No. 21
0022-538X/06/$08.00+0     doi:10.1128/JVI.00631-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Tax Abolishes Histone H1 Repression of p300 Acetyltransferase Activity at the Human T-Cell Leukemia Virus Type 1 Promoter{triangledown}

Kasey L. Konesky, Jennifer K. Nyborg, and Paul J. Laybourn*

Department of Biochemistry and Molecular Biology, Colorado State University, Fort Collins, Colorado 80523-1870

Received 29 March 2006/ Accepted 8 August 2006

Upon infection of human T-cell leukemia virus type 1 (HTLV-1), the provirus is integrated into the host cell genome and subsequently packaged into chromatin that contains histone H1. Consequently, transcriptional activation of the virus requires overcoming the environment of chromatin and H1. To efficiently activate transcription, HTLV-1 requires the virally encoded protein Tax and cellular transcription factor CREB. Together Tax and CREB interact with three cis-acting promoter elements called viral cyclic-AMP response elements (vCREs). Binding of Tax and CREB to the vCREs promotes association of p300/CBP into the complex and leads to transcriptional activation. Therefore, to fully understand the mechanism of Tax transactivation, it is necessary to examine transcriptional activation from chromatin assembled with H1. Using a DNA template harboring the complete HTLV-1 promoter sequence and a highly defined recombinant assembly system, we demonstrate proper incorporation of histone H1 into chromatin. Addition of H1 to the chromatin template reduces HTLV-1 transcriptional activation through a novel mechanism. Specifically, H1 does not inhibit CREB or Tax binding to the vCREs or p300 recruitment to the promoter. Rather, H1 directly targets p300 acetyltransferase activity. Interestingly, in determining the mechanism of H1 repression, we have discovered a previously undefined function of Tax, overcoming the repressive effects of H1-chromatin. Tax specifically abrogates the H1 repression of p300 enzymatic activity in a manner independent of p300 recruitment and without displacement of H1 from the promoter.

* Corresponding author. Mailing address: Department of Biochemistry and Molecular Biology, Colorado State University, 1870 Campus Delivery, Fort Collins, CO 80523-1870. Phone: (970) 491-5100. Fax: (970) 491-0494. E-mail: Paul.Laybourn{at}colostate.edu.

{triangledown} Published ahead of print on 30 August 2006.

Journal of Virology, November 2006, p. 10542-10553, Vol. 80, No. 21
0022-538X/06/$08.00+0     doi:10.1128/JVI.00631-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Sharma, N., Nyborg, J. K. (2008). The coactivators CBP/p300 and the histone chaperone NAP1 promote transcription-independent nucleosome eviction at the HTLV-1 promoter. Proc. Natl. Acad. Sci. USA 105: 7959-7963 [Abstract] [Full Text]  
  • Sharma, N., Lopez, D. I., Nyborg, J. K. (2007). DNA Binding and Phosphorylation Induce Conformational Alterations in the Kinase-inducible Domain of CREB: IMPLICATIONS FOR THE MECHANISM OF TRANSCRIPTION FUNCTION. J. Biol. Chem. 282: 19872-19883 [Abstract] [Full Text]  


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