Epigenetic information is able to interact with the cellular environment and could be especially useful for reprograming gene expression in response to a physiological perturbation. In fact the genes induced or repressed by osmotic stress undergo significant changes in terms of the levels of various histone modifications, especially in the acetylation levels of histone H3. Exposing yeast to high osmolarity results in the activation of stress-activated protein kinase HOG1, which plays a central role in gene expression control. We evaluated the connection between the presence of HOG1 and changes in histone H3 acetylation in stress-regulated genes. We found a parallel increase in the acetylation of lysines 9 and 14 of H3 in induced genes during stress, which was largely dependent on HOG1 at the genome-wide level. Conversely, we observed that acetylation decreased in repressed genes and was not dependent on HOG1. However, lack of HOG1 sometimes produced different, and even opposite, effects on the induction and acetylation of H3 of each gene. We also found that the acetylation state of lysine 9 of H3 was altered in the strains deficient in NUT1 HAT and HOS1 HDAC in the genes up-regulated during osmotic stress in an Msn2/Msn4-independent manner, while lysine 9 acetylation of H3 varied in the strains deficient in SAS2 HAT and RPD3 HDAC for the Msn2/Msn4-dependent induced genes. The results presented here show new, unexpected participants in gene regulation processes in response to environmental perturbations.
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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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