All cells, whether free-living or part of a multicellular organism, must contend with a variety of environmental fluctuations that can be harmful or lethal to the cell. Cells exposed to different kinds of environmental stress rapidly alter gene transcription, resulting in the immediate downregulation of housekeeping genes, while crucial stress-responsive transcription is drastically increased. Common cis-acting elements within many stress-induced promoters, such as stress response elements and heat shock elements, allow for coordinated expression in response to many different stresses. However, specific promoter architectures, i.e., specific combinations of high- and low-affinity stress-responsive cis elements embedded in a particular chromatin environment, allow for unique expression patterns that are responsive to the individual type and degree of stress. The coordination of transcriptional stress responses and the role that chromatin structure plays in the regulation and kinetics of such responses is discussed. The interplay among global and gene-specific stress responses is illustrated using the constitutive and stress-induced transcriptional regulation of HSP82 as a model. This review also investigates evidence suggesting that stress-induced transcription is globally synchronized with the stress-induced repression of housekeeping gene via 2 distinct mechanisms of facilitating the binding of TATA-binding protein (TBP): TFIID and SAGA-mediated TBP binding.
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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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