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M201333200v1
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Papers In Press, published online ahead of print October 4, 2002
J. Biol. Chem, 10.1074/jbc.M201333200
Submitted on February 8, 2002
Revised on September 26, 2002
Accepted on October 4, 2002

Multiple mechanisms contribute to the activation of RNA polymerase III transcription in cells transformed by Papovaviruses

Zoe A. Felton-Edkins and Robert J. White

Department of Biochemistry and Molecular Biology, University of Glasgow, Glasgow G12 8QQ

Corresponding Author: rwhite{at}udcf.gla.ac.uk

RNA polymerase (pol) III transcription is abnormally active in fibroblasts transformed by Polyomavirus (Py) or Simian Virus 40 (SV40). Several distinct mechanisms contribute to this effect. In untransformed fibroblasts, the basal pol III factor TFIIIB is repressed through association with the retinoblastoma protein RB; this restraint is overcome by large T antigens of Py and SV40. Furthermore, cells transformed by these papovaviruses overexpress the BDP1 subunit of TFIIIB, at both the protein and mRNA levels. Despite the overexpression of BDP1, the abundance of the other TFIIIB components is unperturbed following papovavirus transformation. In contrast, mRNAs encoding all five subunits of the basal factor TFIIIC2 are found at elevated levels in fibroblasts transformed by Py or SV40. Thus, both papovaviruses stimulate pol III transcription by boosting production of selected components of the basal machinery. Py differs from SV40 in encoding a highly oncogenic middle T antigen that localizes outside the nucleus and activates several signal transduction pathways. Middle T can serve as a potent activator of a pol III reporter in transfected cells. Several distinct mechanisms therefore contribute to the high levels of pol III transcription that accompany transformation by Py and SV40.


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