Under stress, cells need to optimize the activity of a wide range of gene products during the response phases: shock, adaptation, and recovery. This requires coordination of several levels of regulation, including turnover and translation efficiencies of mRNAs. Mitogen-activated protein (MAP) kinase pathways are implicated in many aspects of the environmental stress response, including initiation of transcription, translation efficiency, and mRNA turnover. In this study, we analyze mRNA turnover rates and mRNA steady-state levels at different time points following mild hyperosmotic shock in Saccharomyces cerevisiae cells. The regulation of mRNA stability is transient and affects most genes for which there is a change in transcript level. These changes precede and prepare for the changes in steady-state levels, both regarding the initial increase and the later decline of stress-induced mRNAs. The inverse is true for stress-repressed genes, which become stabilized during hyperosmotic stress in preparation of an increase as the cells recover. The MAP kinase Hog1 affects both steady-state levels and stability of stress-responsive transcripts, whereas the Hog1-activated kinase Rck2 influences steady-state levels without a major effect on stability. Regulation of mRNA stability is a wide-spread, but not universal, effect on stress-responsive transcripts during transient hyperosmotic stress. By destabilizing stress-induced mRNAs when their steady-state levels have reached a maximum, the cell prepares for the subsequent recovery phase when these transcripts are to return to normal levels. Conversely, stabilization of stress-repressed mRNAs permits their rapid accumulation in the recovery phase. Our results show that mRNA turnover is coordinated with transcriptional induction.
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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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| Evidence ID | Analyze ID | File | Description |
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