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Molecular and Cellular Biology, July 1999, p. 4927-4934, Vol. 19, No. 7
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Activation of RNA Polymerase III Transcription in Cells Transformed by Simian Virus 40

Christopher G. C. Larminie, Josephine E. Sutcliffe, Kerrie Tosh, Andrew G. Winter, Zoe A. Felton-Edkins, and Robert J. White*

Institute of Biomedical and Life Sciences, Division of Biochemistry and Molecular Biology, University of Glasgow, Glasgow G12 8QQ, United Kingdom

Received 19 February 1999/Returned for modification 24 March 1999/Accepted 16 April 1999

RNA polymerase (Pol) III transcription is abnormally active in fibroblasts that have been transformed by simian virus 40 (SV40). This report presents evidence that two separate components of the general Pol III transcription apparatus, TFIIIB and TFIIIC2, are deregulated following SV40 transformation. TFIIIC2 subunits are expressed at abnormally high levels in SV40-transformed cells, an effect which is observed at both protein and mRNA levels. In untransformed fibroblasts, TFIIIB is subject to repression through association with the retinoblastoma protein RB. The interaction between RB and TFIIIB is compromised following SV40 transformation. Furthermore, the large T antigen of SV40 is shown to relieve repression by RB. The E7 oncoprotein of human papillomavirus can also activate Pol III transcription, an effect that is dependent on its ability to bind to RB. The data provide evidence that both TFIIIB and TFIIIC2 are targets for activation by DNA tumor viruses.


* Corresponding author. Mailing address: Institute of Biomedical and Life Sciences, Division of Biochemistry and Molecular Biology, Davidson Building, University of Glasgow, Glasgow G12 8QQ, United Kingdom. Phone: 0141-330-4628. Fax: 0141-330-4620. E-mail: rwhite{at}udcf.gla.ac.uk.


Molecular and Cellular Biology, July 1999, p. 4927-4934, Vol. 19, No. 7
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.



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