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Journal of Virology, July 2001, p. 6498-6507, Vol. 75, No. 14
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.14.6498-6507.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Transactivation of Murine Cyclin A by Polyomavirus Large and Small T Antigens

Stefan Schüchner, Maria Nemethova, Aurelia Belisova, Britta Klucky, Wolfgang Holnthoner, and Erhard Wintersberger*

Department of Medical Biochemistry, Division of Molecular Biology, University of Vienna, A-1030 Vienna, Austria

Received 29 January 2001/Accepted 16 April 2001

Polyomavirus large and small T antigens cooperate in the induction of S phase in serum-deprived Swiss 3T3 cells. While the large T antigen is able to induce S phase-specific enzymes, we have recently shown that both T antigens contribute to the production of the cyclins E and A and that the small T antigen is essential for the induction of cyclin A-dependent cdk2 activity (S. Schüchner and E. Wintersberger, J. Virol. 73:9266-9273, 1999). Here we present our attempts to elucidate the mechanisms by which the large and the small T antigens transactivate the murine cyclin A gene. Using Swiss 3T3 cells carrying the T antigens and various mutants thereof under the hormone-inducible mouse mammary tumor virus promoter, as well as transient-cotransfection experiments with the T antigens and cyclin A promoter-luciferase reporter constructs, we found the following. The large T antigen activates the cyclin A promoter via two transcription factor binding sites, a cyclic AMP responsive element (CRE), and the major negative regulatory site called CDE-CHR. While an intact binding site for pocket proteins is required for the function of this T antigen at the CDE-CHR, its activity at the CRE is largely independent thereof. In contrast, an intact J domain and an intact zinc finger are required at both sites. The small T antigen also appears to have an influence on the cyclin A promoter through the CRE as well as the CDE-CHR. For this an interaction with protein phosphatase 2A is essential; mutation of the J domain does not totally eliminate but greatly reduces the transactivating ability.

* Corresponding author. Mailing address: Department of Medical Biochemistry, Division of Molecular Biology, University of Vienna, Dr. Bohr-Gasse 9, A-1030 Vienna, Austria. Phone: 43-1-4277-61704. Fax: 43-1-4277-61705. E-mail: Wi{at}mol.univie.ac.at.

Journal of Virology, July 2001, p. 6498-6507, Vol. 75, No. 14
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.14.6498-6507.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:

  • Dahl, J., Chen, H. I., George, M., Benjamin, T. L. (2007). Polyomavirus Small T Antigen Controls Viral Chromatin Modifications through Effects on Kinetics of Virus Growth and Cell Cycle Progression. J. Virol. 81: 10064-10071 [Abstract] [Full Text]  
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