@article{mbs:/content/journal/jgv/10.1099/0022-1317-78-9-2259, author = "Marriott, Susan J. and Payne, Kimberly and Connor, Laurie M.", title = "Augmentation of human T cell leukaemia virus type I Tax transactivation by octamer binding sites", journal= "Journal of General Virology", year = "1997", volume = "78", number = "9", pages = "2259-2267", doi = "https://doi.org/10.1099/0022-1317-78-9-2259", url = "https://www.microbiologyresearch.org/content/journal/jgv/10.1099/0022-1317-78-9-2259", publisher = "Microbiology Society", issn = "1465-2099", type = "Journal Article", abstract = "The human T cell leukaemia virus type I (HTLV-I) 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.", }