Analysis of the UGA3-GLT1 bidirectional promoter has indicated that its transcriptional activation is determined by the combined action of Gcn4p and Gln3p, and that its bidirectional character is influenced by chromatin organization, through the action of an Abf1p binding site and a polydAdT(tract). Results presented in this paper show that lack of Gcn5p impairs histone acetylation and nucleosomal organization of the UGA3-GLT1 promoter, resulting in an asymmetrical transcriptional activation response of UGA3 and GLT1. The phenotype displayed by a double mutant impaired in GCN5 and in the Abf1p binding site indicates that the combined action of these two elements determines the bidirectional capacity of the UGA3-GLT1 intergenic region.
|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||Reference||Annotation Extension|
|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||Conditions||Strain||Source||Reference|