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Nucleic Acids Research, 1989, Vol. 17, No. 14 5737-5749
© 1989

MOLECULAR BIOLOGY

Studies of heterologous promoter trans-activation by the HTLV-II tax protein

Janice L. Williams, Alan J. Cann, Todd Leff, Paolo Sassone-Corsi and Irvin S.Y. Chen

Division of Hematology-Oncology, Departments of Medicine and Microbiology and Immunology, UCLA School of Medicine and Jonsson Comprehensive Cancer Center Los Angeles, CA 90024-1678, USA

Received April 18, 1989. Accepted June 14, 1989.

The tax protein of HTLV-II increases the level of steady-state mRNAproduced from the HTLV-II long terminal repeat (LTR) and also activatesheterologous promoters. We have previously shown that the adenovirus E3promoter, which is trans-activated by the adenovirus Ela protein, is also trans-activated by the tax protein. To investigate the mechanism of trans-activation bytax, we analyzed E3 promoter deletion mutants to determinenucleotide sequence requirements for activation of this promoter. Our resultsshow that removal of different upstream regions within the promoter does notresult in loss of trans-activation, Indicating that tax does not appear to interact with a single DNA binding protein to activate the E3 promoter. In addition, tax and Ela together activate the E3 promoter ina greater than additive fashion, suggesting that these proteins function differently.Possible mechanisms of activation by the tax protein are discussed.


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