Journal of General Virology, Vol 78, 2259-2267, Copyright © 1997 by Society for General Microbiology
Augmentation of human T cell leukaemia virus type I Tax transactivation by octamer binding sites
SJ Marriott, K Payne and LM Connor
Division of Molecular Virology, Baylor College of Medicine, Houston, TX 77030, USA. susanm@bcm.tmc.edu
The human T cell leukaemia virus type I (HTLV-1) Tax protein is an
activator of viral and cellular gene expression. Tax does not bind DNA
directly, but does interact with cellular DNA binding proteins. These
interactions bring Tax to a specific group of promoters and may help to
determine the specificity of Tax transactivation. Previous studies have
demonstrated that the activity of Tax, when tethered to a given promoter,
is enhanced by the presence of adjacent transcription factor binding sites.
To examine the specificity of this augmentation, a series of transcription
factor binding sites was tested for the ability to enhance the activity of
a Gal-Tax fusion protein. The greatest increase in Gal-Tax activity was
observed when an octamer binding site was placed adjacent to the Gal4
binding sites. However, the octamer binding site failed to independently
function as a Tax responsive element in the absence of an adjacent
Tax-tethering element. Oct-2 was not required for augmentation of Gal-Tax
activity as this enhancement was observed in BHK-21 cells, which lack
Oct-2. The ability of octamer binding sites to augment transcription was
specific for Gal-Tax, as compared to other transactivators. Taken together,
these results demonstrate that the degree of Tax transactivation can be
influenced by the elemental composition of the target promoter.
