We replaced the required TATA element of a yeast gal-his3 promoter by a binding site for GCN4, a protein that normally activates transcription when bound upstream of a TATA element. Surprisingly, GCN4 efficiently activates his3 transcription from wild-type initiation sites, though in a pattern associated with constitutive his3 transcription rather than GCN4 upstream activation through a TATA element. Transcriptional stimulation by GCN4 requires both the DNA-binding domain and the acidic activation function but is not affected by changing the spacing or helical relationship between the GCN4 binding site and the mRNA start sites. GCN4 is not sufficient for this TATA-independent activation; a sequence in the gal fragment distinct from the GAL4 binding sites is also required. Thus, GCN4 functions both when bound upstream of a TATA element and also when bound at the position of a TATA element. In the latter case, we suggest the possibility that GCN4 might be able to stimulate transcription by an alternate mechanism that does not involve a conventional TATA-binding transcription factor.
|Evidence ID||Analyze ID||Interactor||Interactor Systematic Name||Interactor||Interactor Systematic Name||Type||Assay||Annotation||Action||Modification||Phenotype||Source||Reference||Note|
|Evidence ID||Analyze ID||Gene||Gene Systematic Name||Gene Ontology Term||Gene Ontology Term ID||Qualifier||Aspect||Method||Evidence||Source||Assigned On||Annotation Extension||Reference|
|Evidence ID||Analyze ID||Gene||Gene Systematic Name||Phenotype||Experiment Type||Experiment Type Category||Mutant Information||Strain Background||Chemical||Details||Reference|
|Evidence ID||Analyze ID||Regulator||Regulator Systematic Name||Target||Target Systematic Name||Experiment||Assay||Construct||Conditions||Strain Background||Reference|