Redox-sensitive bZIP68 plays a role in balancing stress tolerance with growth in Arabidopsis
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ABSTRACT:
ORGANISM(S): Arabidopsis thaliana
PROVIDER: GSE133900 | GEO | 2020/07/01
REPOSITORIES: GEO
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2018-11-12 | GSE117478 | GEO
Project description:Engineered abiotic stress resistance is an important target for increasing agricultural productivity.There are concerns, however, regarding possible ecological impacts of transgenic crops. In contrast to the first wave of transgenic crops, many abiotic stress resistance genes can initiate complex downstream changes. Transcriptome profiling has been suggested as a comprehensive non-targeted approach to examine secondary effects. We compared phenotypic and transcriptomic effects of constitutive expression of genes intended to confer salt stress tolerance by three different mechanisms: a transcription factor, CBF3/DREB1a; a metabolic gene, M6PR, for mannitol biosynthesis; and the Na+/H+ antiporter, SOS1. Transgenic CBF3, M6PR, and SOS1 Arabidopsis thaliana were grown together in the growth chamber, greenhouse and field. In the absence of salt, M6PR and SOS1 lines performed comparably to wild type; CBF3 lines exhibited dwarfing as reported previously. All three transgenes conferred fitness advantage when subjected to 100 mM NaCl in the growth chamber. CBF3 and M6PR affected transcription of numerous abiotic stress- related genes as measured by Affymetrix microarray analysis. M6PR additionally modified expression of biotic- and oxidative- stress genes. Transcriptional effects of SOS1 in the absence of salt were smaller and primarily limited to redox-related genes. The extent of transcriptome change, however, did not correlate with effects on growth and reproduction. Thus, magnitude of global transcriptome differences may not predict phenotypic differences upon which environment and selection act to influence fitness. These observations have implications for interpretation of transcriptome analyses in the context of risk assessment and emphasize importance of evaluation within a phenotypic context. Both transgenic plants and relative WT plants were grown in the growth chamber in the absence and presence of salt stress. Plants from 20 days after sowing (6 days after salt treatment) were used for RNA extraction and hybridization on Affymetrix microarrays. There were two biological replicates for each genotype and salt treatment combination.
2011-10-05 | E-GEOD-26983 | biostudies-arrayexpress
Project description:Redox Responsive Transcription Factor1 (RRTF1) in Arabidopsis is rapidly and transiently upregulated by H202, as well as biotic and abiotic induced redox signals. Inactivation of RRTF1 restricts and overexpression promotes reactive oxygen species (ROS) accumulation in response to stress. Overexpressor (oe) lines are impaired in root and shoot development, light sensitive and susceptible to Alternaria brassicae infection. These symptoms are diminished by the beneficial root endophyte Piriformospora indica which reduces ROS accumulation locally in roots and systemically in shoots, and by antioxidants and ROS inhibitors which scavenge ROS. More than 850 stress-, redox-, ROS regulated-, ROS scavenging-, defense-, cell death- and senescence-related genes are regulated by RRTF1, ~ 30% of them have ROS related functions. Bioinformatic analyses and in vitro DNA binding assays demonstrate that RRTF1 binds to GCC-box and GCC-box like sequences in the promoter of RRTF1-responsive genes. Upregulation of RRTF1 by stress stimuli as well as H2O2 requires WRKY18/40/60. RRTF1 is co-regulated with the phylogenetically related RAP2.6, which contains GCC-box like sequene in its promoter, but RAP2.6 oe lines do not accumulate higher ROS levels. RRTF1 stimulates systemic ROS accumulation in distal non-stressed leaves. We conclude that the highly conserved RRTF1 rapidly, transiently and systemically induce ROS accumulation in response to ROS and ROS-producing abiotic and biotic stress signals. Necrotrophs stimulate RRTF1 expression, while symbiotic interactions of Arabidopsis with (hemi)-biotrophs and P. indica do not affect or repress RRTF1 expression. The seedlings were grown on MS medium with 1.37% sucrose under short day conditions and low light intensity (30 µmol m-2s-1) at 20˚C for 14 days. Transcriptome analysis was performed for the rrtf1 knock-out line and a RRTF1-overlexpressor line (called oe18) in comparison to wild-type seedlings.
2015-04-23 | E-GEOD-64783 | biostudies-arrayexpress
Project description:Redox Responsive Transcription Factor1 (RRTF1) in Arabidopsis is rapidly and transiently upregulated by H202, as well as biotic and abiotic induced redox signals. Inactivation of RRTF1 restricts and overexpression promotes reactive oxygen species (ROS) accumulation in response to stress. Overexpressor (oe) lines are impaired in root and shoot development, light sensitive and susceptible to Alternaria brassicae infection. These symptoms are diminished by the beneficial root endophyte Piriformospora indica which reduces ROS accumulation locally in roots and systemically in shoots, and by antioxidants and ROS inhibitors which scavenge ROS. More than 850 stress-, redox-, ROS regulated-, ROS scavenging-, defense-, cell death- and senescence-related genes are regulated by RRTF1, ~ 30% of them have ROS related functions. Bioinformatic analyses and in vitro DNA binding assays demonstrate that RRTF1 binds to GCC-box and GCC-box like sequences in the promoter of RRTF1-responsive genes. Upregulation of RRTF1 by stress stimuli as well as H2O2 requires WRKY18/40/60. RRTF1 is co-regulated with the phylogenetically related RAP2.6, which contains GCC-box like sequene in its promoter, but RAP2.6 oe lines do not accumulate higher ROS levels. RRTF1 stimulates systemic ROS accumulation in distal non-stressed leaves. We conclude that the highly conserved RRTF1 rapidly, transiently and systemically induce ROS accumulation in response to ROS and ROS-producing abiotic and biotic stress signals. Necrotrophs stimulate RRTF1 expression, while symbiotic interactions of Arabidopsis with (hemi)-biotrophs and P. indica do not affect or repress RRTF1 expression. Mature leaves of 5 weeks-old Col-0 wild type and RRTF1-overexpressor Arabidopsis (called oe18), which were grown on soil under short-day condition at 20˚C, were subjected to RNA extraction and Affymetrix microarray analysis. Three biological independent experiments for both Col-0 and oe18 were performed.
2015-04-23 | E-GEOD-64853 | biostudies-arrayexpress
Project description:Pharmacological intervention of redox balance in cancer cells often results in oxidative stress-mediated apoptosis, attracting much attention for the development of a new generation of targeted therapy in cancer. However, little is known about mechanisms underlying the conversion from oxidative signaling to downstream activities leading cells to death. We here report a systematic detection of transcriptome changes in response to oxidative signals generated in leukemia cells upon fenretinide treatment, implicating the occurrence of numerous stress-responsive events during the fenretinide induced apoptosis, such as redox response, endoplasmic reticulum stress/unfolded protein response, translational repression and proteasome activation. Moreover, the configuration of these relevant events is primarily orchestrated by stress responsive transcription factors, as typically highlighted by NF-E2-related factor-2 (NRF2) and heat shock factor 1 (HSF1). Several lines of evidence suggest that the coordinated regulation of these transcription factors and thus their downstream genes are involved in converting oxidative signaling into downstream stress-responsive events regulating pro-apoptotic and apoptotic activities at the temporal and spatial levels, typifying oxidative stress-mediated programmed death rather than survival in cancer cells. This study provides a roadmap for understanding oxidative stress-mediated apoptosis in cancer cells, which may be further developed into more sophisticated therapeutic protocols, as implicated by synergistic induction of cell apoptosis using proteasome inhibitors with fenretinide. Time-series experiment, fenretinide treated NB4 cells at 19 time points (i.e., 0.25, 0.5, 1, 2, 4, 6, 8, 10, 12, 15, 18, 21, 24, 30, 36, 42, 48, 54 and 60 hours) and untreated NB4 cells at 4 time points (i.e., 0, 8, 12 and 15 hours).
2010-05-05 | E-GEOD-16578 | biostudies-arrayexpress
Project description:This is the model with unfitted
parameters described in the article
Dynamic rerouting of the carbohydrate flux is key to counteracting oxidative stress
Markus Ralser, Mirjam M Wamelink, Axel Kowald, Birgit Gerisch, Gino Heeren, Eduard A Struys, Edda Klipp, Cornelis Jakobs, Michael Breitenbach, Hans Lehrach and Sylvia Krobitsch, J Biol
2007 6(4):10; PMID: 18154684
, doi: 10.1186/jbiol61
Abstract:
BACKGROUND: Eukaryotic cells have evolved various response mechanisms to counteract the deleterious consequences of oxidative stress. Among these processes, metabolic alterations seem to play an important role.
RESULTS: We recently discovered that yeast cells with reduced activity of the key glycolytic enzyme triosephosphate isomerase exhibit an increased resistance to the thiol-oxidizing reagent diamide. Here we show that this phenotype is conserved in Caenorhabditis elegans and that the underlying mechanism is based on a redirection of the metabolic flux from glycolysis to the pentose phosphate pathway, altering the redox equilibrium of the cytoplasmic NADP(H) pool. Remarkably, another key glycolytic enzyme, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), is known to be inactivated in response to various oxidant treatments, and we show that this provokes a similar redirection of the metabolic flux.
CONCLUSION: The naturally occurring inactivation of GAPDH functions as a metabolic switch for rerouting the carbohydrate flux to counteract oxidative stress. As a consequence, altering the homoeostasis of cytoplasmic metabolites is a fundamental mechanism for balancing the redox state of eukaryotic cells under stress conditions.
Different realtive enzyme velocities can be simulated by varying the parameters k_rel_TPI
and k_rel_GAPDH
.
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.
To cite BioModels Database, please use Le Novère N., Bornstein B., Broicher A., Courtot M., Donizelli M., Dharuri H., Li L., Sauro H., Schilstra M., Shapiro B., Snoep J.L., Hucka M. (2006) BioModels Database: A Free, Centralized Database of Curated, Published, Quantitative Kinetic Models of Biochemical and Cellular Systems Nucleic Acids Res., 34: D689-D691.
2007-04-11 | BIOMD0000000247 | BioModels
Project description:The OsCPK4 gene is a member of the complex gene family of the Calcium-dependent protein kinases (CPKs) in rice. Expression of OsCPK4 is induced by high salinity, drought and the phytohormone abscisic acid. The OsCPK4 protein localizes to the plasma membrane. Transgenic rice overexpressing OsCPK4 enhances tolerance to salt and drought stress, the transgenic plants having stronger water-holding capability than control plants. Microarray analysis of OsCPK4 rice plants revealed up-regulation of genes involved in metabolism, particularly lipid metabolism, as well as genes involved in oxidative stress and redox control. Meanwhile, OsCPK4 overexpression has no impact on the expression of the well-characterized abiotic stress-associated transcription factors (i.e. DREB and NAC), or the typical salt and drought-inducible genes (i.e. LEA genes, including Dehydrin genes). Under salt stress conditions, the OsCPK4 transgenic lines showed lesser membrane lipid peroxidation as compared to control plants, indicating that OsCPK4 rice plants have a better capacity to prevent oxidative damage in cellular membrane lipids. Collectively, our data suggest that OsCPK4-mediated processes protect the plant cell from uncontrolled redox reactions affecting membrane functions, which, in turn, results in salt and drought tolerance. OsCPK4 shows great promise for genetic improvement of tolerance to abiotic stress in rice.
2014-07-03 | GSE52353 | GEO
Project description:It is well appreciated that reactive oxygen species (ROS) are deleterious to mammals, including humans, especially when generated in abnormally large quantities from cellular metabolism. Whereas the mechanisms leading to the production of ROS are rather well delineated, the mechanisms underlying tissue susceptibility or tolerance to oxidant stress remain elusive. Through an experimental selection over many generations, we have previously generated Drosophila melanogaster flies that tolerate tremendous oxidant stress and have shown that the family of antimicrobial peptides (AMP) is over-represented in these tolerant flies. Furthermore, we have also demonstrated that overexpression of even one AMP at a time (e.g. Diptericin) allows wild type flies to survive much better in hyperoxia. In the current study, we used a number of experimental approaches to investigate the potential mechanisms underlying hyperoxia tolerance in flies with antimicrobial peptide overexpression. We demonstrate that flies with Diptericin overexpression resist oxidative stress by increasing antioxidant enzyme activities and preventing an increase in ROS level after hyperoxia. Depleting the GSH pool using buthionine sulfoximine limits fly survival, thus confirming that enhanced survival observed in these flies is related to improved redox homeostasis. We conclude that a) AMPs play an important role in tolerance to oxidant stress; b) overexpression of Diptericin changes the cellular redox balance between oxidant and antioxidant, and c) this change in redox balance plays an important role in survival in hyperoxia. Expression profiles of Drosophila melanogaster with anti-microbial peptide over-expression (experimental sample; n=3) and controls (UAS-AMP alone not crossed to da-GAL4; n=3) were determined using Affymetrix Drosophila Genome 2.0 Arrays.
2010-12-21 | E-GEOD-23902 | biostudies-arrayexpress
Project description:Protein S-thiolation is a post-translational thiol-modification that controls redox-sensing transcription factors and protects active site cysteine residues against irreversible oxidation. In Bacillus subtilis the MarR-type repressor OhrR was shown to sense organic hydroperoxides via formation of mixed disulfides with the redox buffer bacillithiol (Cys-GlcN-Malate, BSH), termed as S-bacillithiolation. Here, we have studied changes in the transcriptome and redox proteome caused by the strong oxidant hypochloric acid in B. subtilis. The expression profile of NaOCl stress is indiciative of disulfide stess as shown by the induction of the thiol- and oxidative stress-specific Spx, CtsR and PerR regulons. Thiol redox proteomics identified only few cytoplasmic proteins with reversible thiol-oxidations in response to NaOCl stress that include GapA and MetE. Shotgun-LC-MS/MS analyses revealed that GapA, Spx and PerR are oxidized to intramolecular disulfides by NaOCl stress. Furthermore, we identified six S-bacillithiolated proteins in NaOCl-treated cells, including the OhrR repressor, two methionine synthases MetE and YxjG, the inorganic pyrophosphatase PpaC, the 3-D-phophoglycerate dehydrogenase SerA and the putative bacilliredoxin YphP. S-bacillithiolation of the OhrR repressor leads to up-regulation of the OhrA peroxiredoxin that confers together with BSH specific protection against NaOCl. S-bacillithiolation of MetE, YxjG, PpaC and SerA causes hypochlorite-induced methionine starvation as supported by the induction of the S-box regulon. The mechanism of S-glutathionylation of MetE has been described in Escherichia coli also leading to enzyme inactivation and methionine auxotrophy. In summary, our studies discover an important role of the BSH redox buffer in protection against hypochloric acid by S-bacillithiolation of the redox-sensing regulator OhrR and of four enzymes of the methionine biosynthesis pathway.
2011-07-04 | GSE27637 | GEO
Project description:Redox Responsive Transcription Factor1 (RRTF1) in Arabidopsis is rapidly and transiently upregulated by H202, as well as biotic and abiotic induced redox signals. Inactivation of RRTF1 restricts and overexpression promotes reactive oxygen species (ROS) accumulation in response to stress. Overexpressor (oe) lines are impaired in root and shoot development, light sensitive and susceptible to Alternaria brassicae infection. These symptoms are diminished by the beneficial root endophyte Piriformospora indica which reduces ROS accumulation locally in roots and systemically in shoots, and by antioxidants and ROS inhibitors which scavenge ROS. More than 850 stress-, redox-, ROS regulated-, ROS scavenging-, defense-, cell death- and senescence-related genes are regulated by RRTF1, ~ 30% of them have ROS related functions. Bioinformatic analyses and in vitro DNA binding assays demonstrate that RRTF1 binds to GCC-box and GCC-box like sequences in the promoter of RRTF1-responsive genes. Upregulation of RRTF1 by stress stimuli as well as H2O2 requires WRKY18/40/60. RRTF1 is co-regulated with the phylogenetically related RAP2.6, which contains GCC-box like sequene in its promoter, but RAP2.6 oe lines do not accumulate higher ROS levels. RRTF1 stimulates systemic ROS accumulation in distal non-stressed leaves. We conclude that the highly conserved RRTF1 rapidly, transiently and systemically induce ROS accumulation in response to ROS and ROS-producing abiotic and biotic stress signals. Necrotrophs stimulate RRTF1 expression, while symbiotic interactions of Arabidopsis with (hemi)-biotrophs and P. indica do not affect or repress RRTF1 expression.
2015-04-23 | GSE64853 | GEO