GATA family activators (Gln3p and Gat1p) and repressors (Dal80p and Deh1p) regulate nitrogen catabolite repression (NCR)-sensitive transcription in Saccharomyces cerevisiae presumably via their competitive binding to the GATA sequences upstream of NCR-sensitive genes. Ure2p, which is not a GATA family member, inhibits Gln3p/Gat1p from functioning in the presence of good nitrogen sources. We show that NCR-sensitive DAL80 transcription can be influenced by the relative levels of GAT1 and URE2 expression. NCR, normally observed with ammonia or glutamine, is severely diminished when Gat1p is overproduced, and this inhibition is overcome by simultaneously increasing URE2 expression. Further, overproduction of Ure2p nearly eliminates NCR-sensitive transcription under derepressive growth conditions, i.e. with proline as the sole nitrogen source. Enhanced green fluorescent protein-Gat1p is nuclear when Gat1p-dependent transcription is high and cytoplasmic when it is inhibited by overproduction of Ure2p.
|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|