There is a strong relationship between the regulatory pathways to oxidative stress, longevity, and aging. High hydrostatic pressure (HHP) induces oxidative stress and activates cellular defense mechanisms. The understanding of these mechanisms is a strategy to delay damage associated with aging. Addressing resistance to stress and aging in Saccharomyces cerevisiae is a well-accepted approach since pathways involved in energy balance, damage accumulation and stress response are preserved among eukaryotes. The purpose of this study was to correlate the environmental stress response to cell maturity. HHP stress response on S. cerevisiae mother and daughter cells was evaluated through survival, reactive oxygen species (ROS) accumulation and gene expression. Mature cells were yeasts that had budded and originated at least one descendant, and young cells were the ones that did not form a bud. Mature cells were more resistant to HHP, although they showed a decrease in expression of antioxidants enzymes genes, and a higher intracellular levels of ROS. Young cells had less resistance to HHP despite a tendency of positively regulating these same antioxidant encoders. The TOR1 gene, related to aging and apoptosis, was unchanged in mother cells and showed a tendency toward increased expression in daughter cells submitted to HHP. The gene modulation differences of the mother and daughter cells indicates that maturity plays an important role in the HHP stress response and resistance. Thus, even accumulating high levels of ROS, mature cells were more tolerant to HHP stress and survived better, despite aging.
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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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