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J Biol Chem, Vol. 273, Issue 23, 14119-14129, June 5, 1998

Molecular Mechanisms of Promoter Regulation of the gp34 Gene That Is Trans-activated by an Oncoprotein Tax of Human T Cell Leukemia Virus Type I

Kiyoshi Ohtani, Atsumi Tsujimoto, Tomonori Tsukahara^§, Noboru Numata^¶, Shigeto Miura^**, Kazuo Sugamura, and Masataka Nakamura

From the  Human Gene Sciences Center and the ^§ Department of Immunotherapeutics, Medical Research Division, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8510, the ^¶ Department of Microbiology, Sendai Municipal Institute of Public Health, 2-5-10 Oroshimachi-higashi, Wakabayashi-ku, Sendai 983-0002, the  Department of Microbiology and Immunology, Tohoku University School of Medicine, 2-1 Seiryo-machi, Aoba-ku, Sendai 980-8575, and ^** Core Research for Evolutional Science and Technology, Japan Science and Technology Corp., 4-1-8 Honcho, Kawaguchi 332-0012, Japan

We investigated the molecular mechanism of transcriptional activation of the gp34 gene by the Tax oncoprotein of human T cell leukemia virus type I (HTLV-I). gp34 is a type II transmembrane molecule belonging to the tumor necrosis factor family and is constitutively expressed on HTLV-I-producing cells but not normal resting T cells. The transcriptional regulatory region of the gp34 gene was activated by HTLV-I Tax in the human T cell line Jurkat, in which endogenous gp34 is induced by Tax. Sequence analysis demonstrated that two NF-B-like elements (1 and 2) were present in the regulatory region. Both NF-B-like elements were able to bind to NF-B or its related factor(s) in a Tax-dependent manner. Chloramphenicol acetyltransferase assays indicated that NF-B-like element 1 was Tax-responsive, although the activity was lower than that the native promoter. NF-B-like element 2 elevated promoter activity when combined with NF-B-like element 1, indicating cooperative function of the elements for maximum promoter function. Unlike typical NF-B elements, the NF-B-like elements in gp34 were not activated by treatment of Jurkat cells with phorbol ester despite induction of the NF-B-like binding activity. Chloramphenicol acetyltransferase reporter assays using the region upstream of the NF-B-like elements identified an upstream region that reduced transcription from cognate and noncognate core promoters in a Tax-independent manner. Our results imply complex regulation of expression of the gp34 gene and suggest implication of gp34 in proliferation of HTLV-I infected T cells.

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