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Transcription profiling of Arabidopsis under hydrogen peroxide stress overexpressing Zat12

ABSTRACT: In this experiment we tested the transcriptome of transgenic Arabidopsis seedlings (5-day-old) constitutively expressing the zinc-finger protein Zat12 (At5g59820) under the control of the 35S-CaMV promoter (Zat12). The transcriptome of these seedlings was compared to that of wild type seedlings grown under the same conditions (WT) and to that of wild type seedlings grown under the same conditions and subjected to a hydrogen peroxide stress (WT+H2O2). Hydrogen peroxide treatment was performed by applying 20 mM hydrogen peroxide for 1 hour. In parallel to these experiments transgenic plants expressing Zat12 were subjected to a similar hydrogen peroxide stress (Zat12+H2O2). All treatments were performed with similar size and age seedlings grown in liquid culture (MS) and sampled at the same time as described by Davletova et al., 2005. Experimenter name = Ron Mittler; Experimenter phone = 1-775-784-1384; Experimenter fax = 1-775-784-1650; Experimenter department = Dept. of Biochemistry; Experimenter institute = University of Nevada; Experimenter address = MS200; Experimenter address = Reno; Experimenter address = Nevada; Experimenter zip/postal_code = 89557; Experimenter country = USA Experiment Overall Design: 12 samples were used in this experiment

ORGANISM(S): Arabidopsis thaliana

SUBMITTER: Nottingham Arabidopsis Stock Centre (NASC)

PROVIDER: E-GEOD-5530 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Hydrogen peroxide stress and Zat12 over-expression in Arabidopsis.

Project description:In this experiment we tested the transcriptome of transgenic Arabidopsis seedlings (5-day-old) constitutively expressing the zinc-finger protein Zat12 (At5g59820) under the control of the 35S-CaMV promoter (Zat12). The transcriptome of these seedlings was compared to that of wild type seedlings grown under the same conditions (WT) and to that of wild type seedlings grown under the same conditions and subjected to a hydrogen peroxide stress (WT+H2O2). Hydrogen peroxide treatment was performed by applying 20 mM hydrogen peroxide for 1 hour. In parallel to these experiments transgenic plants expressing Zat12 were subjected to a similar hydrogen peroxide stress (Zat12+H2O2). All treatments were performed with similar size and age seedlings grown in liquid culture (MS) and sampled at the same time as described by Davletova et al., 2005. Experimenter name = Ron Mittler Experimenter phone = 1-775-784-1384 Experimenter fax = 1-775-784-1650 Experimenter department = Dept. of Biochemistry Experimenter institute = University of Nevada Experimenter address = MS200 Experimenter address = Reno Experimenter address = Nevada Experimenter zip/postal_code = 89557 Experimenter country = USA Keywords: genetic_modification_design; stimulus_or_stress_design

2006-08-15 | GSE5530 | GEO

Over-expression of MBF1c enhances stress tolerance

Project description:Multiprotein bridging factor 1c MBF1c (At3g24500) is a stress-response transcription co-activator. To test the function of MBF1c, we over-expressed it in transgenic Arabidopsis plants using the 35S-CaMV promoter. T4 seeds form 3 independent lines were tested for their tolerance to biotic and abiotic stress conditions. Constitutive expression of MBF1c in Arabidopsis enhanced the tolerance of transgenic plants to bacterial infection, salinity, heat and osmotic stress. Moreover, the enhanced tolerance of transgenic plants to osmotic and heat stress was maintained even when these two stresses were combined. The expression of MBF1c in transgenic plants augmented the accumulation of a number of sugars and defense transcrtipts in response to heat stress. Transcriptome profiling and inhibitor studies suggest that MBF1c expression enhances the tolerance of transgenic plants to heat and osmotic stress by partially activating, or perturbing, the ethylene-response signal transduction pathway. MBF1 proteins could be used to enhance the tolerance of plants to different abiotic stresses. Suzuki et al., 2005 Plant Physiology, submitted. Experimenter name = Ron Mittler Experimenter phone = 1-775-784-1384 Experimenter fax = 1-775-784-1650 Experimenter department = Dept. of Biochemistry Experimenter institute = University of Nevada Experimenter address = MS200 Experimenter address = Reno Experimenter address = Nevada Experimenter zip/postal_code = 89557 Experimenter country = USA Keywords: genetic_modification_design; stimulus_or_stress_design

2006-08-15 | GSE5539 | GEO

Over-expression of MBF1c enhances stress tolerance

Project description:Multiprotein bridging factor 1c MBF1c (At3g24500) is a stress-response transcription co-activator. To test the function of MBF1c, we over-expressed it in transgenic Arabidopsis plants using the 35S-CaMV promoter. T4 seeds form 3 independent lines were tested for their tolerance to biotic and abiotic stress conditions. Constitutive expression of MBF1c in Arabidopsis enhanced the tolerance of transgenic plants to bacterial infection, salinity, heat and osmotic stress. Moreover, the enhanced tolerance of transgenic plants to osmotic and heat stress was maintained even when these two stresses were combined. The expression of MBF1c in transgenic plants augmented the accumulation of a number of sugars and defense transcrtipts in response to heat stress. Transcriptome profiling and inhibitor studies suggest that MBF1c expression enhances the tolerance of transgenic plants to heat and osmotic stress by partially activating, or perturbing, the ethylene-response signal transduction pathway. MBF1 proteins could be used to enhance the tolerance of plants to different abiotic stresses. Suzuki et al., 2005 Plant Physiology, submitted. Experimenter name = Ron Mittler; Experimenter phone = 1-775-784-1384; Experimenter fax = 1-775-784-1650; Experimenter department = Dept. of Biochemistry; Experimenter institute = University of Nevada; Experimenter address = MS200; Experimenter address = Reno; Experimenter address = Nevada; Experimenter zip/postal_code = 89557; Experimenter country = USA Experiment Overall Design: 6 samples were used in this experiment

2008-06-13 | E-GEOD-5539 | biostudies-arrayexpress

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2016-06-10 | E-GEOD-80200 | biostudies-arrayexpress

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2012-09-05 | GSE40574 | GEO

Expression data from Arabidopsis under hydrogen peroxide and light treatment

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2012-09-05 | E-GEOD-40574 | biostudies-arrayexpress

Adaptation to hydrogen peroxide

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2009-04-23 | GSE12602 | GEO

Respiratory burst oxidase homologues D and F in catalase2 deficient plants

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2016-06-10 | GSE81516 | GEO

Expression data of H2O2 responding genes at Arabidopsis root tip

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2018-07-31 | GSE85015 | GEO

Genome-wide transcriptome analysis of the oxygen response of L. johnsonii reveals that NADH oxidase is a secondary H2O2 source.

Project description:Oxidative stress due to endogenous hydrogen peroxide production by Lactobacillus species is a well-known issue in the food industry. In this study, the transcriptional response to oxygen of Lactobacillus johnsonii, one of the H2O2-producing strains used in the food industry, was analyzed. It was found that aerobic growth conditions led to a more than two-fold downregulation of 45 genes as compared to anaerobic growth, whereas 6 genes were more than twofold upregulated. Among the upregulated genes were two genes that displayed significant homology to NADH-dependent oxidoreductase (NOX). The postulated transcriptional regulation of the nox promoter by oxygen was studied using a GUS-reporter construct, confirming a 2.1-fold upregulated GUS-expression upon aerobic growth. Exposure to sublethal levels of hydrogen peroxide did not result in significant regulation of the nox promoter. In a previous study of hydrogen peroxide production by L. johnsonii, a NADH flavin reductase (NFR) was identified to be involved in hydrogen peroxide production. An NFR-deficient derivative was strongly impaired in H2O2 production, but regained a partial H2O2 producing capacity upon prolonged oxygen exposure. The nox-promoter appeared to be 3.6-fold upregulated under aerobic conditions in the NFR-deficient background, which may imply a role of this gene in the regained H2O2 production. Indeed, deletion of the nox-gene in the NFR-deletion background, resulted in a strain that no longer produced H2O2, also during prolonged exposure to oxygen. The double-mutant (nfr, nox) displayed strongly impaired aerobic growth and oxygenation induced rapid growth stagnation that is not caused by H2O2. We conclude that H2O2 production in L. johnsonii is primarily dependent on NFR but can also involve an oxygen-inducible NADH oxidase under aerobic conditions. Moreover, our results imply that H2O2 production plays a prominent role in oxygen tolerance of L. johnsonii.

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