The addition of glucose to derepressed cells of the yeast Saccharomyces cerevisiae triggers activation of the cAMP pathway with a rapid drop in stress resistance as a consequence. We have isolated the LRE1 gene as a multicopy suppressor of glucose-induced loss of heat resistance. Overexpression of LRE1 in a wild-type strain causes the same phenotype as observed in strains with reduced activity of the cAMP-PKA pathway: higher heat resistance and enhanced trehalose levels. Deletion of LRE1 results in the opposite phenotypes. Epistasis analysis indicates that these effects are independent of cAMP and PKA, of the protein kinases Yak1, Sch9 and Rim15 and of the transcription factors Msn2 and Msn4. Lre1 has recently been isolated in a two-hybrid screen using the conserved protein kinase Cbk1 as a bait. Cbk1 controls the expression of CTS1 (encoding chitinase) through the transcription factor Ace2. We demonstrate here that overexpression of LRE1 represses CTS1 whereas deletion of LRE1 induces the expression of CTS1. Repression of CTS1 results in deficient cell separation as a result of inefficient degradation of the chitin ring after cytokinesis. Neither deletion nor overexpression of LRE1 has any effect on CTS1 expression in a cbk1Delta mutant, indicating that Lre1 inhibits Cbk1. In addition, we show that increased trehalose accumulation and increased heat resistance caused by overexpression of LRE1 are also the result of inhibition of Cbk1, revealing a novel control pathway for certain targets affected by PKA. The yeast genome contains a homologue of LRE1, YDR528w, which we have called HLR1 (for homologue of Lre1). Deletion and overexpression of HLR1 causes similar but less pronounced effects compared with LRE1.
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Evidence ID | Analyze ID | Gene/Complex | Systematic Name/Complex Accession | Qualifier | Gene Ontology Term ID | Gene Ontology Term | Aspect | Annotation Extension | Evidence | Method | Source | Assigned On | Reference |
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Evidence ID | Analyze ID | Gene | Gene Systematic Name | Phenotype | Experiment Type | Experiment Type Category | Mutant Information | Strain Background | Chemical | Details | Reference |
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Evidence ID | Analyze ID | Gene | Gene Systematic Name | Disease Ontology Term | Disease Ontology Term ID | Qualifier | Evidence | Method | Source | Assigned On | Reference |
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Evidence ID | Analyze ID | Regulator | Regulator Systematic Name | Target | Target Systematic Name | Direction | Regulation of | Happens During | Regulator Type | Direction | Regulation Of | Happens During | Method | Evidence | Strain Background | Reference |
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Site | Modification | Modifier | Source | Reference |
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Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Allele | Assay | Annotation | Action | Phenotype | SGA score | P-value | Source | Reference | Note |
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Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Assay | Annotation | Action | Modification | Source | Reference | Note |
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Complement ID | Locus ID | Gene | Species | Gene ID | Strain background | Direction | Details | Source | Reference |
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Evidence ID | Analyze ID | Dataset | Description | Keywords | Number of Conditions | Reference |
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