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Journal of Virology, October 2008, p. 9359-9368, Vol. 82, No. 19
0022-538X/08/$08.00+0     doi:10.1128/JVI.00242-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Transcriptional Control of Spliced and Unspliced Human T-Cell Leukemia Virus Type 1 bZIP Factor (HBZ) Gene{triangledown}

Mika Yoshida,1 Yorifumi Satou,1 Jun-ichirou Yasunaga,1 Jun-ichi Fujisawa,2 and Masao Matsuoka1*

Laboratory of Virus Control, Institute for Virus Research, Kyoto University, 53 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan,1 Department of Microbiology, Kansai Medical University, 15-10 Fumizono-cho, Moriguchi, Osaka 570-8506, Japan2

Received 3 February 2008/ Accepted 11 July 2008

The human T-cell leukemia virus type 1 (HTLV-1) basic leucine zipper factor (HBZ) gene is encoded by the minus strand of the HTLV-1 provirus and transcribed from the 3' long terminal repeat (LTR). HBZ gene expression not only inhibits the Tax-mediated activation of viral gene transcription through the 5' LTR but also promotes the proliferation of infected cells. However, the HBZ promoter region and the transcriptional regulation of the gene have not been studied. In this study, we characterize the promoters of the spliced version of the HBZ gene (sHBZ) and the unspliced version of the HBZ gene (usHBZ) by luciferase assay. Both promoters were TATA-less and contained initiators and downstream promoter elements. Detailed studies of the promoter for the sHBZ gene showed that Sp1 sites were critical for its activity. The activities of the sHBZ and usHBZ gene promoters were upregulated by Tax through Tax-responsible elements in the 3' LTR. We compared the functions of the proteins derived from the sHBZ and usHBZ transcripts. sHBZ showed a stronger suppression of Tax-mediated transcriptional activation through the 5' LTR than did usHBZ; the level of suppression correlated with the level of protein produced. The expression of sHBZ had a growth-promoting function in a T-cell line, while usHBZ expression did not. This study demonstrates that Sp1 is critical for sHBZ transcription, which accounts for the constitutive expression of the sHBZ gene. Functional differences between sHBZ and usHBZ suggest that the sHBZ gene plays a significant role in the proliferation of infected cells.

* Corresponding author. Mailing address: Laboratory of Virus Control, Institute for Virus Research, Kyoto University, 53 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan. Phone: 81-75-751-4048. Fax: 81-75-751-4049. E-mail: mmatsuok{at}virus.kyoto-u.ac.jp

{triangledown} Published ahead of print on 23 July 2008.

Journal of Virology, October 2008, p. 9359-9368, Vol. 82, No. 19
0022-538X/08/$08.00+0     doi:10.1128/JVI.00242-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



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