Retrograde signalling during caused by heritable mitochondrial dysfunction is partly mediated by ANAC017 and improves plant performance.
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB14313 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR1447070.fastq.gz | Fastqsanger.gz | |||
| ERR1447080.fastq.gz | Fastqsanger.gz | |||
| ERR1447071.fastq.gz | Fastqsanger.gz | |||
| ERR1447081.fastq.gz | Fastqsanger.gz | |||
| ERR1447072.fastq.gz | Fastqsanger.gz |
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Similar Datasets
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.
2016-07-28 | E-MTAB-4655 | biostudies-arrayexpress
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
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.
2013-01-30 | GSE41136 | GEO
Project description:Retrograde signaling from the chloroplast to the nucleus is necessary to regulate the chloroplast proteome during development and fluctuating environmental conditions. Although the specific chloroplast process(es) that must occur and the nature of the signal(s) that exits the chloroplast are not well understood, previous studies using drug inhibitors of chloroplast biogenesis have revealed that normal chloroplast development is required to express Photosynthesis Associated Nuclear Genes (PhANGs). In an attempt to determine which specific steps in chloroplast development are involved in retrograde signaling, we analyzed Arabidopsis mutants defective in the six genes encoding sigma factor (Sig) proteins that are utilized by the plastid-encoded RNA polymerase to transcribe specific sets of plastid genes. Here, we demonstrate that both Sig2 and Sig6 have partially redundant roles in not only plastid transcription, but also tetrapyrrole synthesis and retrograde signaling to control PhANG expression. Normal PhANG expression can be partly restored in the sig2 mutant by increasing heme synthesis. Furthermore, there is a genetic interaction between Sig and GUN (genomes uncoupled) genes to generate chloroplast-retrograde signals. These results demonstrate that defective plastid transcription is the source of at least two retrograde signals to the nucleus; one involving tetrapyrrole synthesis and the other involving the accumulation of an unknown plastid transcript. We also propose that the study of sig mutants (with defects in the expression of specific plastid genes) provides a new genetic system, which avoids the use of harsh inhibitors and their potential side effects, to monitor developmental retrograde signaling and to elucidate its mechanisms.
2012-09-18 | E-MTAB-4338 | biostudies-arrayexpress
Project description:Strigolactones (SL) are a new class of plant hormones with a broad range of roles in symbiosis, germination and developmental regulation. The well-characterized signaling pathway for SL involves the canonical signaling component MAX2. Here we identified a novel, MAX2-independent SL signaling mechanism, which initiates in mitochondria, signals to the nucleus and regulates root development. By a forward genetic approach, we identified the SL-insensitive pig1 mutant, which altered the kinetic properties of the mitochondrial pyruvate dehydrogenase complex. SL has an unknown target in mitochondria, where it uncouples respiration. This leads to metabolic aberrations, mitochondria-to-nucleus retrograde signaling upregulating transcription of mitochondrial dysfunction genes and downregulating auxin-regulated genes. SL-triggered mitochondrial uncoupling is communicated to the nucleus via cleavage and translocation of the ER-localized transcription factor ANAC017. These observations establish a novel mechanism for SL signaling emanating from mitochondria and regulating development.
2022-04-18 | GSE200634 | GEO
Project description:Environmental variation is commonplace, but unpredictable. Populations that encounter a deleterious environment can sometimes avoid extinction by rapid evolutionary adaptation. Phenotypic variability, whereby a single genotype can express multiple different phenotypes, might play an important role in rescuing such populations from extinction. This type of evolutionary bet-hedging need not confer a direct benefit to a single individual, but it may increase the chance of long-term survival of a lineage. Here, we develop a population genetic model to explore how partly heritable phenotypic variability influences the probability of evolutionary rescue and the mean duration of population persistence in changing environments. We find that the probability of population persistence depends nonmonotonically on the degree of phenotypic heritability between generations: some heritability can help avert extinction, but too much heritability removes any benefit of phenotypic variability. Partly heritable phenotypic variation is particularly advantageous when it extends the persistence time of a declining population and thereby increases the chance of rescue via beneficial mutations at linked loci. We discuss the implications of these results in the context of therapies designed to eradicate populations of pathogens or aberrant cellular lineages.
| S-EPMC6404248 | biostudies-other
Project description:Distinct retrograde signaling pathways have been identified for several cellular organelles. These pathways are important to maintain the function of these organelles in response to organelle-specific stress. Using Caenorhabditis elegans, we show for the first time that such a retrograde signaling also exists for peroxisomes. Analysis of the C. elegans transcriptome revealed that peroxisomal import stress caused by the knock-down of the peroxisomal matrix protein import receptor prx-5/PEX5 induces the compensatory up-regulation of genes involved in defense response and lipid metabolic processes, especially peroxisomal beta oxidation. We, therefore, propose that the peroxisomal retrograde signaling participates in the maintenance of peroxisomal function in response to peroxisomal import stress.
2020-12-19 | GSE156318 | GEO
Project description:Peroxisomal retrograde signaling in C. elegans
| PRJNA657442 | ENA
Project description:Signals originating within plastids modulate organelle differentiation by transcriptionally regulating nuclear-encoded genes. These retrograde signals are also integral regulators of plant development, including leaf morphology. The clb5 mutant displays severe leaf morphology defects due to Apocarotenoid Signal 1 (ACS1) accumulation in the developmentally arrested plastid. Transcriptomic analysis of clb5 validates ACS1 as a true retrograde signal impacting expression of hundreds of nuclear genes, including suppression of most genes encoding plastid ribosomal proteins.
2021-06-02 | GSE152252 | GEO
Project description:While retrograde signalling pathways have been identified for several organelles, the existence of such a pathway for peroxisomes remains elusive. We identified a peroxisomal retrograde signalling (PRS) in C. elegans, which is activated in response to peroxisomal import stress. We analyzed the PRS using a proteomic approach.
2021-01-11 | PXD014720 | Pride