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J. Biol. Chem., Vol. 279, Issue 51, 52978-52983, December 17, 2004

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Enhanced Activation of Tax-dependent Transcription of Human T-cell Leukemia Virus Type I (HTLV-I) Long Terminal Repeat by TORC3^*

Hiroshi Koga, Takayuki Ohshima, and Kunitada Shimotohno¶

From the Department of Viral Oncology, Institute for Virus Research, Kyoto University, Sakyo-ku, Kyoto 606-8502, Japan

Tax, a protein encoded by the env-pX gene of human T-cell leukemia virus type I (HTLV-I), interacts with various host cell transcription factors. Tax activates transcription from the long terminal repeat (LTR) of HTLV-I through association with cyclic AMP-responsive element-binding protein (CREB). Here, we present evidence that transducer of regulated cyclic AMP-response element-binding protein 3 (TORC3), a co-activator of CREB, is involved in Tax-induced transcriptional activation from the HTLV-I LTR. By using a luciferase assay system, we show that TORC3 alone can enhance transcription from the HTLV-I LTR, as well as from a cellular cyclic AMP-response element (CRE). Interestingly, we find that co-expression of TORC3 and Tax dramatically increased transcriptional activation at the HTLV-I LTR. We also show by glutathione S-transferase pull-down and co-immunoprecipitation experiments that TORC3 interacts with Tax. Using deletion mutant analysis, we identify the Tax interaction domain of TORC3 as a region spanning from amino acid 1 to 103, which contains a coiled-coil domain. These results provide important clues toward understanding the molecular mechanism of Tax-dependent transcriptional activation of the HTLV-I LTR.

Received for publication, August 6, 2004 , and in revised form, September 27, 2004.

^* This work was supported by grants-in-aid for scientific research from the Ministry of Education, Culture, Sports, Science, and Technology and by grants-in-aid for cancer research and the Second-term Comprehensive 10-year Strategy for Cancer Control from the Ministry of Health, Labor, and Welfare of Japan. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Both authors equally contributed to this work.

A recipient of a Research Resident Fellowship from the Viral Hepatitis Research Foundation of Japan.

^¶ To whom correspondence should be addressed. Tel.: 81-75-7514000; Fax: 81-75-751-3998; E-mail address: kshimoto{at}virus.kyoto-u.ac.jp.

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