Expression data for Saccharomyces cerevisiae oxidative stress response
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ABSTRACT:
ORGANISM(S): Saccharomyces cerevisiae
PROVIDER: GSE7645 | GEO | 2007/10/24
SECONDARY ACCESSION(S): PRJNA99763
REPOSITORIES: GEO
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Project description:Oxidative stress is a harmful condition in a cell, tissue, or organ, caused by an imbalnace between reactive oxygen species and other oxidants and the capacity of antioxidant defense systems to remove them. The budding yeast S. cerevisiae has been the major eukaryotic model for studies of response to oxidative stress. We used microarrays to study the genome-wide temporal response of the yeast S. cerevisiae to oxidative stress induced by cumene hydroperoxide. Keywords: time course
2013-12-17 | GSE26169 | GEO
Project description:Oxidative stress is a harmful condition in a cell, tissue, or organ, caused by an imbalnace between reactive oxygen species and other oxidants and the capacity of antioxidant defense systems to remove them. The budding yeast S. cerevisiae has been the major eukaryotic model for studies of response to oxidative stress. We used microarrays to study the genome-wide temporal response of the yeast S. cerevisiae to oxidative stress induced by cumene hydroperoxide. Keywords: time course The effects of oxidative stress induced by CHP on the transcriptional profile of S. cerevisiae was studied from a dynamical perspective. Yeast cultures were grown in controlled batch conditions, in 1 L fermentors. Three replicate cultures in mid-exponential phase were exposed to 0.19 mM CHP, while three non-treated cultures were used as controls. Samples were collected at t=0 (immediately before adding CHP) and at 3, 6, 12 and 20 min after adding the oxidant. Samples were processed for RNA extraction and profiled using Affymetrix Yeast Genome S98 arrays.
2013-12-17 | E-GEOD-26169 | biostudies-arrayexpress
Project description:Oxidative stress is a harmful condition in a cell, tissue, or organ, caused by an imbalnace between reactive oxygen species and other oxidants and the capacity of antioxidant defense systems to remove them. The budding yeast S. cerevisiae has been the major eukaryotic model for studies of response to oxidative stress. We used microarrays to study the genome-wide temporal response of the yeast S. cerevisiae to oxidative stress induced by cumene hydroperoxide. Experiment Overall Design: The effects of oxidative stress induced by CHP on the transcriptional profile of S. cerevisiae was studied from a dynamical perspective. Yeast cultures were grown in controlled batch conditions, in 1 L fermentors. Three replicate cultures in mid-exponential phase were exposed to 0.19 mM CHP, while three non-treated cultures were used as controls. Samples were collected at t=0 (immediately before adding CHP) and at 3,6,12,20,40,70 and 120 min after adding the oxidant. Samples were processed for RNA extraction and profiled using Affymetrix Yeast Genome S98 arrays.
2008-06-15 | E-GEOD-7645 | biostudies-arrayexpress
Project description:We studied transcriptional responses of the fission yeast Schizosaccharomyces pombe to different intensities of H2O2 stress as well as two other oxidants: menadione sodium bisulfite and tert-butyl hydroperoxide. DNA microarrays were used to study the changes in expression profiles and the transcriptional regulation. We compare and contrast global expression and regulation of different intensities of H2O2 stress and different oxidants. The transcriptional response to low doses of H2O2 is very similar to menadione sodium bisulfite and the genes were controlled primarily by the transcription factor Pap1. The transcriptional response to medium and high doses of H2O2 is very similar to tert-butyl hydroperoxide and the genes were mostly regulated by the stress-activated MAP kinase Sty1p and the transcription factor Atf1p. We also compare global regulation of oxidative stress genes in fission and budding yeasts and discuss evolutionary implications.
2007-12-07 | E-MEXP-1083 | biostudies-arrayexpress
Project description:The early signaling events involved in oxidant recognition and triggering of oxidant-specific defense mechanisms to counteract oxidative stress still remains largely elusive. Our discovery driven comparative proteomics analysis revealed unique early signaling response of yeast Saccharomyces cerevisiae on proteome level to oxidants with different mechanism of action as early as 3 min after treatment with four oxidants, namely H2O2, cumene hydroperoxide (CHP), menadione and diamide, when protein abundances were compared using label-free quantification relying on a high-resolution mass analyzer (Orbitrap). We identified significant regulation of 196 proteins in response to H2O2, 569 proteins in response to CHP, 369 proteins in response to menadione and 207 proteins in response to diamide. Only 17 proteins were common across all treatments, but several more proteins were shared between two or three oxidants. Pathway analyses revealed that each oxidant triggered unique signaling mechanism associated with cell survival and repair. Signaling pathways mostly regulated by oxidants were Ran, mTOR, Rho, and eIEF2. Furthermore, each oxidant regulated these pathways in a unique way indicating specificity of response to oxidants having different mode of action. We hypothesize that interplay of these signaling pathway may be important in recognizing different oxidants to trigger different downstream MAPK signaling cascades and induce specific responses.
2021-01-04 | PXD022685 | Pride
Project description:Oxidative stress is experienced by all aerobic organisms and results in cellular damage. The damage caused during oxidative stress is particular to the oxidant challenge faced, and so too is the induced stress response. The eukaryote Saccharomyces cerevisiae is sensitive to low concentrations of the lipid hydroperoxide - linoleic acid hydroperoxide (LoaOOH) - and its response is unique relative to other peroxide treatments. Part of the yeast response to LoaOOH includes a change in the cellular requirement for nutrients, such as sulfur, nitrogen and various metal ions. The metabolism of sulfur is involved in antioxidant defence, although the role nitrogen during oxidative stress is not well understood. Investigating the response induced by yeast to overcome LoaOOH exposure, with a particular focus on nitrogen metabolism, will lead to greater understanding of how eukaryotes survive lipid hydroperoxide-induced stress, and associated lipid peroxidation, which occurs in the presence of polyunsaturated fatty acids. We used genome-wide microarrays to investigate the changes in gene expression of S. cerevisiae (Dal80M-NM-^T) to LoaOOH-induced oxidative stress. S. cerevisiae (Dal80M-NM-^T) were exposed to an arresting concentration of LoaOOH (75 M-BM-5M) for 1 hr to induce oxidative stress. Yeast treated with an equivalent volume of solvent (methanol) were used as a control. Following treatment conditions, total RNA was extracted from LoaOOH-treated or control yeast and hybridised onto Affymetrix microarrays.
2014-02-13 | E-GEOD-54951 | biostudies-arrayexpress
Project description:Oxidative stress is experienced by all aerobic organisms and results in cellular damage. The damage caused during oxidative stress is particular to the oxidant challenge faced, and so too is the induced stress response. The eukaryote Saccharomyces cerevisiae is sensitive to low concentrations of the lipid hydroperoxide - linoleic acid hydroperoxide (LoaOOH) - and its response is unique relative to other peroxide treatments. Part of the yeast response to LoaOOH includes a change in the cellular requirement for nutrients, such as sulfur, nitrogen and various metal ions. The metabolism of sulfur is involved in antioxidant defence, although the role nitrogen during oxidative stress is not well understood. Investigating the response induced by yeast to overcome LoaOOH exposure, with a particular focus on nitrogen metabolism, will lead to greater understanding of how eukaryotes survive lipid hydroperoxide-induced stress, and associated lipid peroxidation, which occurs in the presence of polyunsaturated fatty acids. We used genome-wide microarrays to investigate the changes in gene expression of S. cerevisiae (Dal80Δ) to LoaOOH-induced oxidative stress.
2014-02-13 | GSE54951 | GEO
Project description:Background: During gut colonization, the enteric pathogen C. jejuni has to surmount the toxic effects of reactive oxygen species produced by its own metabolism, by the host immune system and by the intestinal microflora. Elucidation of C. jejuni oxidative stress defense mechanisms is critical for understanding Campylobacter pathophysiology. Results: The mechanisms of oxidative stress defenses in Campylobacter jejuni were characterized by transcriptional profiling, genes mutagenesis, and phenotypic analysis. The transcriptome changes, in response to H2O2, cumene hydroperoxide, or menadione exposure, were found to be oxidant specific and revealed the differential expression of genes belonging to a variety of biological pathways, from the classical oxidative stress defense systems, to the heat shock response, DNA repair and metabolism, fatty acid and capsule biosynthesis, and multidrug efflux pumps. To define the peroxide sensing regulator PerR, an isogenic mutant was constructed and its transcriptome profile compared to the wild-type strain. Sixty-six genes were found to belong to the PerR regulon. PerR appear to regulate gene expression both dependently and independently of the presence of iron and/or H2O2. The perR mutant was affected in its motility and attenuated in the chick colonization model. Mutagenic and phenotypic studies of the superoxide disumutase SodB, the alkyl-hydroxyperoxidase AhpC, and the catalase KatA, revealed their role in oxidative stress defenses and chick gut colonization. Conclusion: This study reveals the interplay between PerR, the iron metabolism and the oxidative stress defenses and highlights their role in the colonization and/or survival of C. jejuni in the chick cecum. Keywords: Transcriptional response to 3 oxidants (H2O2, menadione and cumene hydroperoxide) and characterization of the perR regulon (comparison of the transciptomes from the wild-type and perR mutant).
2010-09-07 | GSE13126 | GEO
Project description:Background: During gut colonization, the enteric pathogen C. jejuni has to surmount the toxic effects of reactive oxygen species produced by its own metabolism, by the host immune system and by the intestinal microflora. Elucidation of C. jejuni oxidative stress defense mechanisms is critical for understanding Campylobacter pathophysiology. Results: The mechanisms of oxidative stress defenses in Campylobacter jejuni were characterized by transcriptional profiling, genes mutagenesis, and phenotypic analysis. The transcriptome changes, in response to H2O2, cumene hydroperoxide, or menadione exposure, were found to be oxidant specific and revealed the differential expression of genes belonging to a variety of biological pathways, from the classical oxidative stress defense systems, to the heat shock response, DNA repair and metabolism, fatty acid and capsule biosynthesis, and multidrug efflux pumps. To define the peroxide sensing regulator PerR, an isogenic mutant was constructed and its transcriptome profile compared to the wild-type strain. Sixty-six genes were found to belong to the PerR regulon. PerR appear to regulate gene expression both dependently and independently of the presence of iron and/or H2O2. The perR mutant was affected in its motility and attenuated in the chick colonization model. Mutagenic and phenotypic studies of the superoxide disumutase SodB, the alkyl-hydroxyperoxidase AhpC, and the catalase KatA, revealed their role in oxidative stress defenses and chick gut colonization. Conclusion: This study reveals the interplay between PerR, the iron metabolism and the oxidative stress defenses and highlights their role in the colonization and/or survival of C. jejuni in the chick cecum. Keywords: Transcriptional response to 3 oxidants (H2O2, menadione and cumene hydroperoxide) and characterization of the perR regulon (comparison of the transciptomes from the wild-type and perR mutant). To investigate the transcriptional responses of C. jejuni to oxidant exposure, hydrogen peroxide (H2O2), cumene hydroperoxide (CHP), or menadione sodium bisulfite (MND) was added to the 50 ml broth at a final concentration of 1 mM. The same amount of water or DMSO was added to the bacterial culture that served as reference samples for the transcriptional profile study in response to H2O2, MND or CHP. Furthermore, to investigate the transcriptional response of C. jejuni to H2O2 exposure in the presence of excess iron, ferrous sulfate was added to the bacterial culture at a final concentration of 40 µM, 15 min prior to H2O2 exposure. Ten minutes after the addition of the oxidant, total RNA was extracted and processed for microarray hybridization. To identify the PerR regulon, the wild-type strain C. jejuni NCTC 11168 and the perR mutant were grown in 500 ml flasks containing 250 ml of MEMα medium. At mid-log phase, 50 ml of the cultures were transferred to 100 ml flasks and ferrous sulfate and/or H2O2 were added . Ten minutes following the addition of H2O2 the cells were collected and the total RNA extracted.
2010-09-07 | E-GEOD-13126 | biostudies-arrayexpress
Project description:Reactive oxygen species, generated in vivo or exogenously encountered, constantly challenge living organisms. Oxidation of polyunsaturated fatty acids (PUFA), which are susceptible to oxidant attack, can lead to initiation of lipid peroxidation and in turn rapid production of toxic lipid hydroperoxides. Eukaryotic microorganisms such as Saccharomyces cerevisiae can survive harsh industrial conditions that contain high levels of the PUFA linoleic acid and its oxidised derivative, linoleic acid hydroperoxide (LoaOOH). The precise signalling and response mechanisms induced by yeast to overcome lipid hydroperoxide stress are ill understood. We used genome-wide microarrays to investigate the changes in gene expression of S. cerevisiae to LoaOOH-induced oxidative stress. S. cerevisiae (BY4743) were exposed to an arresting concentration of LoaOOH (75 M-BM-5M) for 1 hr to induce oxidative stress. Yeast treated with an equivalent volume of solvent (methanol) were used as a control. Following treatment conditions, total RNA was extracted from LoaOOH-treated or control yeast and hybridised onto Affymetrix microarrays.
2013-06-12 | E-GEOD-47820 | biostudies-arrayexpress