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 transformatio
n. TFIIIC2 subunits are expressed at abnormally high levels in SV40-transfo
rmed cells, an effect which is observed at both protein and mRNA levels. In
untransformed fibroblasts, TFIIIB is subject to repression through associa
tion with the retinoblastoma protein RE. The interaction between RE and TFI
IIB is compromised following SV40 transformation. Furthermore, the large T
antigen of SV40 is shown to relieve repression by RE. The E7 oncoprotein of
human papillomavirus can also activate Pol III transcription, an effect th
at is dependent on its ability to bind to RE. The data provide evidence tha
t both TFIIIB and TFIIIC2 are targets for activation by DNA tumor viruses.