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A role of the TATA box and the general co-activator hTAF_II130/135 in promoter-specific trans-activation by simian virus 40 small t antigen

Petter Angell Olsen

Ole Morten Seternes

Department of Biochemistry, Section for Molecular Genetics, Institute of Medical Biology, University of Tromsø, N-9037 Tromsø, Norway

Correspondence
Ugo Moens
ugom{at}fagmed.uit.no

The small t antigen (st-ag) of simian virus 40 can exert pleiotropic effects on biological processes such as DNA replication, cell cycle progression and gene expression. One possible mode of achieving these effects is through stimulation of NFB-responsive genes encoding growth factors, cytokines, transcription factors and cell cycle regulatory proteins. Indeed, a previous study has shown that st-ag enhanced NFB-mediated transcription. This study demonstrates that promoters possessing a consensus TATA box (i.e. TATAAAAG) in the context of either NFB- or Sp1-binding sites are trans-activated by st-ag. Overexpressing the general transcription factor hTAF_II130/135, but not hTAF_II28 or hTAF_II80, stimulated the activity of promoters in a consensus TATA box-dependent mode. Converting the consensus TATA motif into a non-consensus TATA box strongly impaired activation by st-ag and hTAF_II130/135. Conversely, mutating a non-consensus TATA motif into the consensus TATA box rendered the mutated promoter inducible by st-ag and hTAF_II130/135. Mutation of the TATA box had no effect on TNF- or RelA/p65-mediated induction of NFB-responsive promoters, indicating a specific st-ag effect on hTAF_II130/135. St-ag stimulated the intrinsic transcriptional activity of hTAF_II130/135. Substitutions in the conserved HPDKGG motif in the N-terminal region or a mutation that impaired the interaction with protein phosphatase 2A abrogated the ability of st-ag to activate hTAF_II130/135-mediated transcription. These results indicate that trans-activation of promoters by st-ag may depend on a consensus TATA motif and suggest that such promoters recruit the general transcription factor hTAF_II130/135.

Present address: The National Hospital, Institute of Microbiology, Section for Gene Therapy, N-0027 Oslo, Norway.

Present address: Department of Pharmacology, Institute of Medical Biology, University of Tromsø, N-9037 Tromsø, Norway.

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