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Journal of Virology, December 2002, p. 11960-11970, Vol. 76, No. 23
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.23.11960-11970.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Differential Regulation of the Inhibitor of Apoptosis ch-IAP1 by v-rel and the Proto-Oncogene c-rel

Jarmila Kralova,^1,2 Andrew S. Liss,¹ William Bargmann,¹ Cullen Pendleton,¹ Janani Varadarajan,¹ Emin Ulug,¹ and Henry R. Bose, Jr.^1*

Section of Molecular Genetics and Microbiology and the Institute of Cellular and Molecular Biology, University of Texas at Austin, Austin, Texas 78712-1095,¹ Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, 166 37 Prague 6, Czech Republic²

Received 2 May 2002/ Accepted 23 August 2002

The v-rel oncogene encoded by reticuloendotheliosis virus is the acutely transforming member of the Rel/NF-B family of transcription factors. v-Rel is a truncated and mutated form of c-Rel and transforms cells by inducing the aberrant expression of genes regulated by Rel/NF-B proteins. The expression of ch-IAP1, a member of the inhibitor-of-apoptosis family, is highly elevated in cells expressing v-Rel and contributes to the immortalization of cells transformed by this oncoprotein. In this study we demonstrate that the elevated expression of ch-IAP1 in v-Rel-expressing cells is due to an increased rate of transcription. The ch-IAP1 promoter was isolated, and four Rel/NF-B binding sites were identified upstream of the transcription start site. Two B sites proximal to the transcription start site were required for v-Rel to activate the ch-IAP1 promoter. While c-Rel also utilized these sites, a third more-distal B site was required for its full activation of the ch-IAP1 promoter. Differences in the transactivation domains of v-Rel and c-Rel are responsible for their different abilities to utilize these sites and account for their differential activation of the ch-IAP1 promoter. Although c-Rel was a more potent activator of the ch-IAP1 promoter than v-Rel in transient reporter assays, cells stably overexpressing c-Rel failed to maintain high levels of ch-IAP1 expression. The reduction of ch-IAP1 expression in these cells correlated with the efficient regulation of c-Rel by IB. The ability of v-Rel to escape IB regulation allows for the gradual and sustained elevation of ch-IAP1 expression directly contributing to the transforming properties of v-Rel.

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* Corresponding author. Mailing address: Section of Molecular Genetics and Microbiology, University of Texas at Austin, Austin, TX 78712-1095. Phone: (512) 471-5525. Fax: (512) 471-2130. E-mail: bose{at}mail.utexas.edu.

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Journal of Virology, December 2002, p. 11960-11970, Vol. 76, No. 23
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.23.11960-11970.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

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