The SWR1-Complex dependent deposition of the histone variant Htz1 on promoter nucleosomes is typical of yeast genes whose expression is frequently reprogrammed. Although this epigenetic marking is of significant physiological importance, the determinants of Htz1 deposition, the conditions that set off SWR1-C occupancy and the implications of Htz1 in transcriptional initiation are issues that remain unresolved. In this report we addressed these questions by investigating the GAL1 promoter. We show that Htz1 is required for efficient Mediator recruitment and transcription only when the GAL1 promoter is under the influence of the Tup1 co repressor. In fact we show that it is Tup1 that specifies Htz1 deposition for the promoter nucleosome covering the transcription start site. This deposition occurs rapidly following transcriptional repression and it correlates with a Tup1 independent transient recruitment of the SWR1-Complex. We propose that Tup1 co-operates with SWR1-C and specifies Htz1 deposition at GAL1 thereby marking the promoter for rapid neutralization from its repressive effects.
|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|