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Role of thioredoxin reductase in the Yap1p-dependent response to oxidative stress

ABSTRACT: The Saccharomyces cerevisiae Yap1p transcription factor is required for the H2O2-dependent activation of many antioxidant genes including the TRX2 gene encoding thioredoxin 2. To identify factors that regulate Yap1p activity, we carried out a genetic screen for mutants that show elevated expression of a TRX2-HIS3 fusion in the absence of H2O2. Two independent mutants isolated in this screen carried mutations in the TRR1 gene encoding thioredoxin reductase. Northern blot and whole-genome expression analysis revealed that the basal expression of most Yap1p targets and many other H2O2-inducible genes is elevated in Deltatrr1 mutants in the absence of external stress. In Deltatrr1 mutants treated with H2O2, the Yap1p targets, as well as genes comprising a general environmental stress response and genes encoding protein-folding chaperones, are hyperinduced. However, despite the elevated expression of genes encoding antioxidant enzymes, Deltatrr1 mutants are extremely sensitive to H2O2. The results suggest that cells lacking thioredoxin reductase have diminished capacity to detoxify oxidants and/or to repair oxidative stress-induced damage and that the thioredoxin system is involved in the redox regulation of Yap1p transcriptional activity. Groups of assays that are related as part of a time series. Keywords: time_series_design

ORGANISM(S): Saccharomyces cerevisiae

PROVIDER: GSE2977 | GEO | 2005/07/22

SECONDARY ACCESSION(S): PRJNA91923

REPOSITORIES: GEO

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Transcription profiling of mutations in the yeast TRR1 gene encoding thioredoxin reductase

Project description:The Saccharomyces cerevisiae Yap1p transcription factor is required for the H2O2-dependent activation of many antioxidant genes including the TRX2 gene encoding thioredoxin 2. To identify factors that regulate Yap1p activity, we carried out a genetic screen for mutants that show elevated expression of a TRX2-HIS3 fusion in the absence of H2O2. Two independent mutants isolated in this screen carried mutations in the TRR1 gene encoding thioredoxin reductase. Northern blot and whole-genome expression analysis revealed that the basal expression of most Yap1p targets and many other H2O2-inducible genes is elevated in Deltatrr1 mutants in the absence of external stress. In Deltatrr1 mutants treated with H2O2, the Yap1p targets, as well as genes comprising a general environmental stress response and genes encoding protein-folding chaperones, are hyperinduced. However, despite the elevated expression of genes encoding antioxidant enzymes, Deltatrr1 mutants are extremely sensitive to H2O2. The results suggest that cells lacking thioredoxin reductase have diminished capacity to detoxify oxidants and/or to repair oxidative stress-induced damage and that the thioredoxin system is involved in the redox regulation of Yap1p transcriptional activity.

2005-06-30 | E-SMDB-2716 | biostudies-arrayexpress

Role of thioredoxin reductase in the Yap1p-dependent response to oxidative stress

2005-07-22 | E-GEOD-2977 | biostudies-arrayexpress

Saccharomyces cerevisiae

Project description:Role of thioredoxin reductase in the Yap1p-dependent response to oxidative stress

| PRJNA91923 | ENA

Cytoprotective Nrf2 pathway is induced in chronically Txnrd1-deficient hepatocytes

Project description:Metabolically active cells require robust mechanisms to combat oxidative stress. The cytoplasmic thioredoxin reductase/thioredoxin (Txnrd1/Txn1) system maintains reduced protein dithiols and provides electrons to some cellular reductases, including peroxiredoxins. Here we generated mice in which the txnrd1 gene, encoding Txnrd1, was specifically disrupted in all parenchymal hepatocytes. Keywords: Triplicate comparisons, two conditions.

2009-06-03 | GSE16381 | GEO

Transcription profiling of mouse with txnrd1 specifically disrupted in all parenchymal hepatocytes - reveals cytoprotective Nrf2 pathway is induced in chronically Txnrd1-deficient hepatocytes

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Transcriptome analysis in HT29 and SW480 cells depleted of Prdx2

Project description:Prdx2 is the thioredoxin-dependent peroxidase that reduces H2O2 using reducing power NADPH in the presence of thioredoxin and thioredoxin reductase. Prdx2 plays an important role in growth. factor signaling in mammlian cells. Therefore, we examined the gene expression in colon adenocarcinoma cell line HT29 after Prdx2 depletion. Prdx2 depletion resulted in a significant alteration on gene expression, including protein synthesis, metabolisms, and cell cycle.

2017-05-13 | GSE81429 | GEO

Functions and adaptive responses to oxidative stress of the thioredoxin and glutathione pathways in Clostridium acetobutylicum

Project description:Oxidative stress is harmful for organism and occurs when the cells exposed to superoxid, hydrogen peroxide and alkylhydroperoxides. In microorganism, the glutathione- and thioredoxin-dependent reduction systems are universal and play an important role in response to defending oxidative stress. The _-glutamylcysteine synthetase (_-GCS) is an essential enzyme to biosynthesize the tripeptide glutathione (GSH) in organism. Similarly, thioredoxin reductase is an important enzyme in thioredoxin-dependent reduction system. In Clostridium acetobutylicum, the _-glutamylcysteine synthetase (encoded by CAC1539, gcs) and thioredoxin reductase (encoded by CAC1548, trxB) were inactivated using ClosTron technology. The gcs mutant grew insufficiently and consumed less glucose in the phosphate-limited continuous culture and exhibited more sensitive to oxidative stress. The trxB mutant just exhibited lower growth rate and less glucose uptake in the solventogenic phase, compared to wild type. The DNA microarrays were performed to investigate the transcripome difference between wild type and the mutants. In gcs mutant, the genes related to chemotaxis and flagella biosynthesis proteins were induced significantly and in the trxB mutant, the sporulation genes were induced largely. Based on the phenotypes and transcriptome comparison results, the relationship between GSH- and Trx-dependent induction systems was discussed in Clostridium acetobutylicum.

2015-04-13 | E-MTAB-2747 | biostudies-arrayexpress

comparison ws vs de and dy-Impact of a plastidial redox perturbation on Arabidopsis transcriptome

Project description:af47_thioredoxins - comparison ws vs de and dy - Knock-out mutants of the ferredoxin-thioredoxin reductase were used to evaluate the impact of the redox perturbation of the plastidial thioredoxins on Arabidopsis transcriptome. - Wild-type (WS) and two T-DNA mutant lines for the variable subunit of ferredoxin:thioredoxin reductase ( DY and DE from INRA of Versailles collection) were compared Keywords: wt vs mutant comparison

2007-06-20 | GSE7978 | GEO

Deletion of thioredoxin reductase disrupts redox homeostasis and impairs β-cell function

Project description:Reactive oxygen species (ROS) have been implicated as mediators of pancreatic β-cell damage. While β-cells are thought to be vulnerable to oxidative damage, we have shown, using inhibitors and acute depletions, that thioredoxin reductase, thioredoxin, and peroxiredoxins are the primary mediators of antioxidant defense in β-cells. However, the role of this antioxidant cycle in maintaining redox homeostasis and β-cell survival in vivo remains unclear. Here, we generated mice with a β-cell specific knockout of thioredoxin reductase 1 (Txnrd1.fl/fl; Ins1.Cre/+, βKO). Despite blunted glucose-stimulated insulin secretion, knockout mice maintain normal whole body glucose homeostasis. Unlike pancreatic islets with acute Txnrd1 inhibition, βKO islets do not demonstrate increased sensitivity to continuous ROS. RNA-sequencing analysis revealed that Txnrd1-deficient β-cells have increased expression of Nuclear factor erythroid 2-related factor 2 (Nrf2)-regulated genes, and altered expression of genes involved in heme and glutathione metabolism, suggesting an adaptive response. Txnrd1-deficient β-cells also have decreased expression of factors controlling β-cell function and identity which may explain the mild functional impairment. Together, these results suggest that Txnrd1-knockout β-cells compensate for loss of this essential antioxidant pathway by increasing expression of Nrf2-regulated antioxidant genes, allowing for protection from excess ROS at the expense of normal β-cell function and identity.

2022-07-05 | GSE200965 | GEO

Brown adipose TRX2 deficiency activates mtDNA-NLRP3 to impair thermogenesis and protect against diet-induced insulin resistance

Project description:Brown adipose tissue (BAT), a crucial heat-generating organ, regulate whole-body energy metabolism by mediating thermogenesis. BAT inflammation is implicated in the pathogenesis of mitochondrial dysfunction and impaired thermogenesis. However, the link between BAT inflammation and systematic metabolism remains unclear. Herein, we sought whether BAT inflammation regulates systematic metabolism and thermogenesis. By using mice with BAT deficiency of thioredoxin-2 (TRX2), a protein that scavenges mitochondrial reactive oxygen species (ROS), we evaluated the impact of BAT inflammation on metabolism and thermogenesis and its underlying mechanism. Our results describe that BAT-specific TRX2 ablation improves systematic metabolic performance via enhancing lipid uptake, which protects mice from diet-induced obesity, hypertriglyceridemia, and insulin resistance. TRX2 deficiency impairs adaptive thermogenesis by suppressing fatty acid oxidation. Mechanistically, loss of TRX2 induces excessive mitochondrial ROS, mitochondrial integrity disruption, and cytosolic release of mitochondrial DNA, which in turn activate aberrant innate immune responses in BAT, including the cGAS-STING and the NLRP3 inflammasome pathways. We identify NLRP3 as a key converging point, as its inhibition reverses both the thermogenesis defect and the metabolic benefits seen under nutrient overload in BAT-specific Trx2-deficient mice. In conclusion, we identify TRX2 as a critical hub integrating oxidative stress, inflammation, and lipid metabolism in BAT; uncovering an adaptive mechanism underlying the link between BAT inflammation and systematic metabolism.

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