1887

Abstract

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 -activated by st-ag. Overexpressing the general transcription factor hTAF130/135, but not hTAF28 or hTAF80, 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 hTAF130/135. Conversely, mutating a non-consensus TATA motif into the consensus TATA box rendered the mutated promoter inducible by st-ag and hTAF130/135. 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 hTAF130/135. St-ag stimulated the intrinsic transcriptional activity of hTAF130/135. 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 hTAF130/135-mediated transcription. These results indicate that -activation of promoters by st-ag may depend on a consensus TATA motif and suggest that such promoters recruit the general transcription factor hTAF130/135.

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2003-07-01
2024-03-28
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