HIV Tat represses transcription through Sp1-like elements in the basal promoter.
MHC class I genes are potently repressed by HIV Tat, which transactivates the HIV LTR. Tat represses class I transcription by binding to complexes associated with a novel promoter element, consisting of Sp1-like DNA binding sites. Transcription by other Sp1-dependent promoters, such as MDR1 and the minimal SV40 promoters, is also repressed by Tat, whereas the human beta-actin promoter is neither activated by Sp1 nor repressed by Tat. Tat repression can be overcome by a strong enhancer element. Thus, the SV40 72 bp enhancer element confers protection from Tat-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.
Howcroft
T K
TK
Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Palmer
L A
LA
Brown
J
J
Rellahan
B
B
Kashanchi
F
F
Brady
J N
JN
Singer
D S
DS
D001483:Base Sequence; D001665:Binding Sites; D004247:DNA / Q000235:genetics; D005786:Gene Expression Regulation; D015696:Gene Products, tat / Q000235:genetics*; D006367:HeLa Cells; D015395:Histocompatibility Antigens Class I / Q000235:genetics / Q000276:immunology*; D006801:Humans; D008969:Molecular Sequence Data; D017354:Point Mutation; D011401:Promoter Regions, Genetic / Q000235:genetics; D014158:Transcription, Genetic / Q000235:genetics; D015533:Transcriptional Activation
D015696:Gene Products, tat; D015395:Histocompatibility Antigens Class I; D004247:DNA