Document Type


Publication Date


Publication Title

Journal of Virology


Geisel School of Medicine


Simian virus 40 (SV40) large tumor antigen (T antigen) stimulates the activity of the SV40 late promoter and a number of cellular and other viral promoters. We have characterized the ability of T antigens with mutations in the DNA-binding domain and within the N-terminal 85 residues to activate the SV40 late promoter. T antigens lacking both nonspecific and sequence-specific DNA-binding activities were able to induce the late promoter. Mutations within the N-terminal 85 residues of T antigen diminished activation by less than twofold. Activation by wild-type and most of the mutant T antigens required intact binding sites for the cellular transcription factor TEF-1 in the late promoter. Curiously, two mutants altered in the N-terminal region and an additional mutant altered in the DNA-binding domain activated a late promoter derivative lacking TEF-1 binding sites, indicating the existence of a TEF-1-independent pathway for activation of the late promoter. A consensus binding site for the TATA binding protein, TBP, was created in variants of late promoters either containing or lacking TEF-1 binding sites. Basal expression was increased by the consensus TBP binding site only when TEF-1 binding sites were present, leading to a reduction in the degree of activation by T antigen. However, activation by a mutant T antigen of the promoter lacking TEF-1 sites was unchanged or slightly enhanced by the consensus TBP binding site. These results suggest that some mutant T antigens can stabilize an interaction between TBP and additional factors bound to the late promoter.

Original Citation

Casaz P, Rice PW, Cole CN, Hansen U. A TEF-1-independent mechanism for activation of the simian virus 40 (SV40) late promoter by mutant SV40 large T antigens. J Virol. 1995;69(6):3501-3509. doi:10.1128/JVI.69.6.3501-3509.1995