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Originally published In Press as doi:10.1074/jbc.M005601200 on October 17, 2000

J. Biol. Chem., Vol. 276, Issue 1, 200-205, January 5, 2001
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Human T-lymphotropic Virus Type I Tax Protein Utilizes Distinct Pathways for p53 Inhibition That Are Cell Type-dependent*

Cynthia A. Pise-Masison, Renaud MahieuxDagger , Michael Radonovich, Hua Jiang, and John N. Brady§

From the Basic Research Laboratory, Virus Tumor Biology Section, NCI, National Institutes of Health, Bethesda, Maryland 20892

p53 plays a pivotal role in transmitting signals from many forms of genotoxic stress to genes and factors that control the cell cycle and apoptosis. We have previously shown that the human T-lymphotropic virus type I Tax protein can inhibit p53 function. Recently we reported that Tax inhibits p53 function in Jurkat cells and mouse embryo fibroblasts through a mechanism involving the nuclear factor kappa B pathway and correlates with phosphorylation on serines 15 and 392 of p53. However, several groups have also observed a mechanism that correlates with p300 binding of Tax. To address this controversy and to determine the mechanism by which Tax inhibits p53 function, we examined the activation functions of Tax required for p53 inhibition. In HeLa and H1299 cells the cAMP-response element-binding protein/activating transcription factor activation function is essential, as demonstrated by the Tax mutants M47 and K88A. In addition, expression of exogenous p300 in H1299 cells allows full recovery of p53 transactivation in the presence of Tax. Consistent with p300 being a limiting factor in H1299, Saos-2, and HeLa cells, we found that the level of endogenous p300 is relatively low in these cells compared with Jurkat cells or the human T-lymphotropic virus type I-infected C81 and MT2 cells. Thus our data suggests that Tax utilizes distinct mechanisms to inhibit p53 function that are cell type-dependent.

* The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Dagger Present address: Institut Pasteur, Unité d'Oncologie Virale, 75724 Paris cedex 15, France.

§ To whom correspondence should be addressed: Bldg. 41/B201, Basic Research Laboratory, NCI, National Institutes of Health, Bethesda, MD 20892. Tel.: 301-496-0986; Fax: 301-496-4951; E-mail: bradyj@mail.nih.gov.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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