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J. Virol. doi:10.1128/JVI.00968-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Activation of the HTLV-I LTR by the Ternary Complex Factor, Elk-1

Department of Molecular Virology and Microbiology, Baylor College of Medicine, MS-385, One Baylor Plaza, Houston, TX 77030

^* To whom correspondence should be addressed. Email: susanm{at}bcm.tmc.edu.

	Abstract

Serum response factor (SRF) was recently shown to bind and activate the human T cell leukemia virus type I (HTLV-I) promoter at bases -116 to -125 relative to the transcription start site. In addition to the SRF binding site (CArG box), serum response elements (SRE) also typically contain a binding site for a member of the ternary complex factor (TCF) family. Here we demonstrate the presence of two TCF binding sites upstream of the viral CArG box. Binding of the TCF family member, Elk-1, to these sites was shown to activate transcription of the promoter. Based on these results, the position of the previously described viral SRE (vSRE) within the HTLV-1 promoter can be extended from -116 to -157, to include the two newly identified TCF sites. Purified Elk-1 bound to a probe containing the vSRE, and this complex formed a ternary complex with SRF. In addition, the complex formed by nuclear extract on this probe contained Elk-1 as shown by EMSA supershift. Both of the predicted TCF sites independently bound Elk-1. Elk-1 activated transcription of the HTLV-I LTR and mutations within either of the TCF sites, or the CArG box, reduced responsiveness of the LTR to Elk-1. Chromatin immunoprecipitation demonstrated that Elk-1 associates with the HTLV-I LTR in vivo. These results identify a functional serum response element within the HTLV-I LTR and suggest that both Elk-1 and SRF play important roles in regulating basal HTLV-I gene expression.