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

ABSTRACT: 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.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE36011 | GEO | 2013/01/28

SECONDARY ACCESSION(S): PRJNA151713

REPOSITORIES: GEO

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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

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

2013-01-30 | GSE41136 | GEO

Retrograde signalling during caused by heritable mitochondrial dysfunction is partly mediated by ANAC017 and improves plant performance.

Project description:Mitochondria are crucial for plant viability and are able to communicate information on their functional status to the cellular nucleus via retrograde signalling, thereby affecting gene expression. It is currently unclear if retrograde signalling in response to constitutive mitochondrial biogenesis defects is mediated by the same pathways as those triggered during acute mitochondrial dysfunction. Furthermore, it is unknown if retrograde signalling can effectively improve plant performance when mitochondrial function is constitutively impaired. Here we show that retrograde signalling in mutants defective in mitochondrial proteins RNA polymerase rpotmp or prohibitin atphb3 can be suppressed by knocking out the transcription factor ANAC017. Genome-wide RNA-seq expression analysis revealed that ANAC017 is almost solely responsible for the most dramatic transcriptional changes common to rpotmp and atphb3 mutants, regulating both classical marker genes such as alternative oxidase 1a (AOX1a) and also previously-uncharacterised DUF295 genes that appear to be new retrograde markers. In contrast, ANAC017 does not regulate intra-mitochondrial gene expression or transcriptional changes unique to either rpotmp or atphb3 genotype, suggesting the existence of currently unknown signalling cascades. The data show that the role of ANAC017 extends beyond common retrograde transcriptional responses and affects downstream protein abundance and enzyme activity of alternative oxidase, as well as steady state energy metabolism in atphb3 plants. Furthermore, detailed growth analysis revealed that ANAC017-dependent retrograde signalling provides benefits for growth and productivity in plants with mitochondrial defects. In conclusion, ANAC017 plays a key role in both biogenic and operational mitochondrial retrograde signalling, and improves plant performance when mitochondrial function is constitutively impaired.

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Inhibition of the mitochondrial electron transport chain by antimycin A in Arabidopsis thaliana

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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

Inhibition of the mitochondrial electron transport chain by antimycin A in Arabidopsis thaliana

Project description:Plant mitochondria signal to the nucleus leading to altered transcription of nuclear genes by a process called mitochondrial retrograde regulation (MRR). MRR is implicated in metabolic homeostasis and responses to stress conditions. Transcriptional consequences on nuclear gene expression of mitochondrial perturbations were examined by a microarray analyses. Expression of 1316 was altered by antimycin A (AA) inhibition of the cytochrome respiratory pathway in leaves of soil grown Arabidopsis plants in the dark for 6 hours. Functional gene category (MapMan) and cluster analyses showed that genes with expression levels affected by perturbation from AA or MFA inhibition were most similarly affected by biotic stresses such as pathogens, not oxidative stresses. Overall, the data provide further evidence for the presence of mtROS-independent MRR signaling, and support the proposed involvement of MRR and mitochondrial function in plant responses to biotic stress. Three independent (bio-replicate) experiments were done using three independent plant samples and independent chemicals in the treatments. For each, approximately 30 plants were used for the treated sample and about 30 plants were used as the control treated sample. Plants were treated with 20 uM antimycin A in 0.01% Tween 20 and incubated in the dark at room temperature (25C) for 6 hours. RNA was isolated from the inhibitor treated and control treated plants and used for microarray experiments. For each independent (bio-replicate) experiment, two microarrays were utilized using Cy3 and Cy5 dye-labeled samples and dye swapping was incorporated- so, minimum of 2 microarrays for each of 3 independent experiments (6 microarrays). In addition, two of the microarrays were duplicated so that a total of 8 slides were used in the data analyses.

2013-01-01 | E-GEOD-29204 | biostudies-arrayexpress

Transcript level responses of Plasmodium falciparum to antimycin A

Project description:Abstract: The mitochondrial electron transport chain is essential to Plasmodium and is the target of the antimalarial drug atovaquone. The mitochondrial genomes of Plasmodium sp. are the most reduced known, and the majority of mitochondrial proteins are encoded in the nucleus and imported into the mitochondrion post-translationally. Many organisms have signalling pathways between the mitochondria and the nucleus to regulate the expression of nuclear-encoded mitochondrially-targeted proteins, for example in response to mitochondrial dysfunction. We have studied the gene expression profiles of synchronous Plasmodium falciparum treated with an LD50 concentration of the complex III inhibitor antimycin A, to investigate whether such pathways exist in the parasite. There was a broad perturbation of gene expression. Some effects were attributable to a delay in the gene expression phase of drug-treated parasites. However, our data also indicated regulation of mitochondrial stress response genes and genes involved in pyrimidine biosynthesis. 3 biological replicates each for treated and untreated: control (1/2000 DMSO) and LD50 antimycin A, respectively. Normalised microarray data for antimycin A-treated parasites were contrasted against untreated (DMSO) controls.

2012-04-19 | E-GEOD-28625 | biostudies-arrayexpress

ACONITASE 3 is part of the ANAC017 transcription factor-dependent mitochondrial dysfunction response

Project description:Mitochondria are tightly embedded within metabolic and regulatory networks that optimize plant performance in response to environmental challenges. The best-known mitochondrial retrograde signaling pathway involves stress-induced activation of the transcription factor NAC DOMAIN CONTAINING PROTEIN 17 (ANAC017), which initiates protective responses to stress-induced mitochondrial dysfunction in Arabidopsis (Arabidopsis thaliana). Post-translational control of the elicited responses, however, 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 key components of stress regulation that are induced by mitochondrial dysfunction. Targeted mass spectrometry-based proteomics revealed that the abundance and phosphorylation of ACO3 increased under stress, which required signaling through ANAC017. Phosphomimetic mutation at ACO3-Ser91 and accumulation of ACO3S91D-YFP promoted the expression of genes related to mitochondrial dysfunction. Furthermore, ACO3 contributed to plant tolerance against UV-B or antimycin A-induced mitochondrial dysfunction. These findings demonstrate that ACO3 is both a target and mediator of mitochondrial dysfunction signaling, and critical for achieving stress tolerance in Arabidopsis leaves.

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