MHC class I genes are potently repressed by HIV Tat, which transactiva
tes the HIV LTR. Tat represses class I transcription by binding to com
plexes associated with a novel promoter element, consisting of Sp1-lik
e DNA binding sites. Transcription by other Sp1-dependent promoters, s
uch as MDR1 and the minimal SV40 promoters, is also repressed by Tat,
whereas the human p-actin promoter is neither activated by Sp1 nor rep
ressed by Tat. Tat repression can be overcome by a strong enhancer ele
ment. Thus, the SV40 72 bp enhancer element confers protection from Ta
t-mediated repression on both the minimal SV40 promoter and the class
I promoter. Surprisingly, Tat can activate the class I promoter in the
presence of both the HIV TAR element and a strong upstream enhancer.
These data demonstrate that Tat differentially affects Sp1-responsive
promoters, depending on promoter architecture.