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Arabidopsis transcription factor ANAC017 is a necessary and central control point for normal transcriptome changes in response to reactive oxygen signals, such as H2O2, and specific mitochondrial retrograde stress signals

ABSTRACT: Stresses that target mitochondrial function lead to altered transcriptional responses for 100-1000s of genes genome wide, and are signalled via retrograde communication pathways within the cell. rao2 mutants contain a mutation in the NAC family transcription factor ANAC017 and cannot induce stress responsive genes (such as the mitochondrial alternative oxidase 1a) in response to mitochondrial dysfunction. We sought to define the global gene network regulated through RAO2 function in response to mitochondrial stress (mimicked through treatment of plants with antimycin A - a specific inhibitor of complex III in the mitochondrial electron transfer chain), and non-specific stress signals such as hydrogen peroxide. We have defined global stress responses that are positively and negatively mediated by RAO2 function, and show that greater than 80% of transcripts that are differentially regulated under H2O2 stress require proper functioning of ANAC017 for a normal stress responses. We used Affymetrix microarray to characterise global gene expression profiles for mutant plants with compromised mitochondrial retrograde signalling (rao2 mutants), to define the genome wide transcriptional network regulated through RAO1 function under mitochondrial stress and hydrogen peroxide stress.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE41136 | GEO | 2013/01/30

SECONDARY ACCESSION(S): PRJNA175902

REPOSITORIES: GEO

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Arabidopsis transcription factor ANAC017 is a necessary and central control point for normal transcriptome changes in response to reactive oxygen signals, such as H2O2, and specific mitochondrial retrograde stress signals

Project description:Stresses that target mitochondrial function lead to altered transcriptional responses for 100-1000s of genes genome wide, and are signalled via retrograde communication pathways within the cell. rao2 mutants contain a mutation in the NAC family transcription factor ANAC017 and cannot induce stress responsive genes (such as the mitochondrial alternative oxidase 1a) in response to mitochondrial dysfunction. We sought to define the global gene network regulated through RAO2 function in response to mitochondrial stress (mimicked through treatment of plants with antimycin A - a specific inhibitor of complex III in the mitochondrial electron transfer chain), and non-specific stress signals such as hydrogen peroxide. We have defined global stress responses that are positively and negatively mediated by RAO2 function, and show that greater than 80% of transcripts that are differentially regulated under H2O2 stress require proper functioning of ANAC017 for a normal stress responses. We used Affymetrix microarray to characterise global gene expression profiles for mutant plants with compromised mitochondrial retrograde signalling (rao2 mutants), to define the genome wide transcriptional network regulated through RAO1 function under mitochondrial stress and hydrogen peroxide stress. rao2 EMS lines, independent T-DNA knock-out lines for ANAC017 (anac017-1), ANAC017 gain of function mutants (anac017-2) and wild type seedlings were grown for 14 days, the optimal stage as defined by forward genetic screens that identifed rao2 mutants. Seedlings were grown on GamborgB5 plates and treated by spraying plants with 50 µM antimycin A (an elicitor of mitochondrial retrograde signalling) or 20mM hydrogen peroxide while mock control samples were sprayed with deionised water. Samples were collected after 3hr of treatment for global expression profiling.

2013-01-30 | E-GEOD-41136 | biostudies-arrayexpress

Cyclin-dependent protein kinase E;1 (CDKE;1) is an essential component for mitochondrial retrograde signalling in Arabidopsis thaliana

Project description:Stresses that target mitochondrial function lead to altered transcriptional responses for 100-1000s of genes genome wide, and are signalled via retrograde signalling pathways within the cell. rao1 mutants contain a mutation in a gene encoding a Cyclin-Dependant Kinase E;1 and cannot induce stress responsive genes (such as the mitochondrial alternative oxidase 1a) in response to mitochondrial dysfunction. We sought to define the global gene network regulated through RAO1 function in response to mitochondrial stress (mimicked through treatment of plants with antimycin A - a specific inhibitor of complex III in the mitochondrial electron transfer chain). We have defined global stress responses that are positively and negatively mediated by RAO1 function, as well as global stress responses to antimycin A treatment that are regulated independently of RAO1. We used Affymetrix microarray to characterise global gene expression profiles for mutant plants with compromised mitochondrial retrograde signalling under stress (rao1 mutants), to define the genome wide transcriptional network regulated through RAO1 function. rao1 and wild type 14-day-old seedlings (the optimal stage as defined by forward genetic screens that identifed rao1 mutants) grown on GamborgB5 plates were treated by spraying plants with 50 µM antimycin A (an elicitor of mitochondrial retrograde signalling) while mock control samples were sprayed with deionised water. Samples were collected after 3hr of treatment for global expression profiling.

2013-01-28 | E-GEOD-36011 | biostudies-arrayexpress

Cyclin-dependent protein kinase E;1 (CDKE;1) is an essential component for mitochondrial retrograde signalling in Arabidopsis thaliana

2013-01-28 | GSE36011 | GEO

Gene expression changes in response to aging compared to heat stress, oxidative stress and ionizing radiation in Drosophila melanogaster

2012-11-19 | GSE42255 | GEO

Gene expression changes in response to aging compared to heat stress, oxidative stress and ionizing radiation in Drosophila melanogaster

Project description:Gene expression changes in response to aging, hyperoxia, hydrogen peroxide, ionizing radiation, and heat stress were compared using microarrays. While aging shared features with each stress, aging was more similar to the stresses most associated with oxidative stress (hydrogen peroxide, hyperoxia, ionizing radiation) than to heat stress. Aging is associated with down-regulation of numerous mitochondrial genes, including electron-transport-chain (ETC) genes and mitochondrial metabolism genes, and a sub-set of these changes was also observed upon hydrogen peroxide stress and ionizing radiation stress. Aging shared the largest number of gene expression changes with hyperoxia. The extensive down-regulation of mitochondrial and ETC genes during aging is consistent with an aging-associated failure in mitochondrial maintenance, which may underlie the oxidative stress-like and proteotoxic stress-like responses observed during aging. Thirty five sample of RNA including Stress Controls (4 replicates), Heat Stress (3 replicates), Ionizing Radiation (4 replicates), Sugar (4 replicates), Hydrogen Peroxide (4 replicates), Young Controls (6 replicates) , Hyperoxia (6 replicates) and Old (4 replicates) adult Drosophila were analysed by Affymetrix microarrays. Stress Controls were used as controls for Heat Stress, Ionizing Radiation, Sugar and Hydrogen Peroxide samples. Young Controls were used as controls for Hyperoxia and Old samples. All flies were male progeny of a cross between Oregon-R wildtype and transgenic strain w[1118];P{w+ rtTA}(3)[E2]/ TM3. Flies lacking the balancer but bearing the transgene were used.

2012-11-19 | E-GEOD-42255 | biostudies-arrayexpress

Transcriptional response of Acinetobacter baumannii to hydrogen peroxide and role of mumR and oxyR in regulating this response

Project description:Acinetobacter baumannii is a Gram-negative opportunistic pathogen that causes multiple infections, including pneumonia, bacteremia, and wound infections. Due to multiple intrinsic and acquired drug-resistance mechanisms, A. baumannii isolates are commonly multi-drug resistant and infections are notoriously difficult to treat. Therefore, it is important to identify mechanisms used by A. baumannii to survive stresses encountered during infection as a means of identifying new drug targets. In this study, we determined the transcriptional response of A. baumannii to hydrogen peroxide stress using RNASequencing. Upon exposure to hydrogen peroxide, A. baumannii differentially transcribes several hundred genes. In this study, we also determined the transcriptional profile of A. baumannii strains with the transcriptional regulators mumR or oxyR genetically inactivated and identified transcriptional differences between these strains and wild-type A. baumannii in response to hydrogen peroxide stress. In doing this, the function of A. baumannii OxyR in hydrogen peroxide stress resistance and regulation of genes required for hydrogen peroxide detoxification was defined. Moreover, the contribution of the uncharacterized regulator MumR to hydrogen peroxide stress resistance was also explored. This work reveals the transcriptome of an important human pathogen in the presence of hydrogen peroxide stress.

2018-11-13 | GSE114130 | GEO

Hydroxyurea protects hippocampal neurons against oxidative, metabolic and excitotoxic stress, and improves spatial memory in a mouse model of Alzheimer’s disease (Rat)

Project description:Alzheimer’s disease (AD) is an age-related neurodegenerative disorder characterized by accumulation of amyloid β-peptide (Aβ) plaques in the brain and decreased cognitive function leading to dementia. We determined if hydroxyurea (HU), a ribonucleotide reductase inhibitor known to activate adaptive cellular stress responses in fibroblasts, could protect rat hippocampal neurons against oxidative-, excitatory-, mitochondrial-, and Aβ-induced stress and if HU treatment could improve learning and memory in a mouse model of AD (APP/PS1 double mutant transgenic mice). HU treatment attenuated the loss of cell viability induced by treatment of hippocampal neurons with hydrogen peroxide, glutamate, rotenone, and Aβ1-42. HU treatment also attenuated reductions of mitochondrial reserve capacity, maximal respiration, and cellular ATP content induced by hydrogen peroxide treatment. In vivo, treatment of APP/PS1 AD mice with HU (45 mg/kg/day) improved spatial memory performance in the hippocampus-dependent Morris water maze task. In summary, HU provides neuroprotection against toxic insults, improves mitochondrial bioenergetics, and improves spatial memory in a mouse model of AD. HU may offer a new therapeutic approach to delay cognitive decline in AD.

2018-09-10 | GSE111941 | GEO

Hydroxyurea protects hippocampal neurons against oxidative, metabolic and excitotoxic stress, and improves spatial memory in a mouse model of Alzheimer’s disease (Mouse)

2018-09-10 | GSE111940 | GEO

Aliivibrio salmonicida LFI1238

Project description:Global responses of Aliivibrio salmonicida to hydrogen peroxide

| PRJNA124277 | ENA

ACONITASE 3 is post-translationally controlled in response to mitochondrial stress signals in Arabidopsis

Project description:Mitochondria are tightly embedded within metabolic and regulatory networks that optimize plant performance upon environmental challenges. The best-known mitochondrial retrograde signaling pathway involves stress-induced activation of the transcription factor ANAC017, which mediates the onset of protective responses upon stress-induced mitochondrial dysfunction in Arabidopsis. Post-translational control of the elicited responses, in contrast, remains poorly understood. Previous studies linked protein phosphatase 2A subunit PP2A-B’γ, a key negative regulator of stress responses, with reversible phosphorylation of ACONITASE 3 (ACO3). Here we report on ACO3 and its phosphorylation at Ser91 as regulatory components induced by mitochondrial dysfunction. Targeted mass spectrometry-based proteomics revealed that the abundance and phosphorylation of ACO3 increased under stress, and that this required signaling through ANAC017. Phosphomimetic mutation at ACO3-Ser91 and the accumulation of ACO3S91D-YFP, in turn, promoted the expression of stress related genes and ACO3 function associated with plant tolerance against UV-B or antimycin A-induced mitochondrial dysfunction. These findings positioned ACO3 both as a target and modulator of mitochondrial dysfunction signaling, critical in the attainment of stress tolerance in Arabidopsis leaves.

2021-06-08 | PXD024316 | Pride

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