Arabidopsis thaliana
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA317230 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Ozone (O3) is a phytotoxic air pollutant that enters the plant through stomata and activates cell death programs leading to development of lesions in sensitive plant species. Exposure to O3 provokes the formation of reactive oxygen species (ROS) in the apoplast of plant cells. Imbalanced ROS homeostasis has deleterious toxic effects on DNA, proteins, lipids, and carbohydrates. However, ROS are not merely damaging molecules, as they also initiate signaling events that help plants acclimate to stress. Like under most abiotic and biotic stresses, apoplastic ROS signaling triggered by O3 induces massive changes in gene expression, enzyme activities and metabolic profiles. Thus, O3 is a very useful tool to study general mechanisms of ROS signaling and regulation of gene expression. Here we used a combination of transcriptome analysis and cell death assays to identify molecular mechanism initiated by apoplastic ROS signaling involved in the regulation of defense signaling and cell death in Arabidopsis thaliana.
2020-07-01 | GSE117052 | GEO
Project description:As sessile organism, plants evolved a highly complicated signaling system to cope with unfavorable and fluctuating environmental conditions. Rapid and transient Reactive Oxygen Species (ROS) burst is a common response to both biotic and abiotic stresses. Plants exposed with O3 could trigger extracellular similar ROS production through cell wall peroxidases and NPADPH oxidases, resulting in changes in the gene expression and cell death. Whereas ROS induced cell death is not simply due to its toxicity, rather due to interplay with several other signaling pathways, such as salicylic acid (SA), jasmonic acid (JA) and ethylene signaling pathways. Furthermore, the three hormones have both synergistic and antagonistic interactions, where the suppression of JA signaling by SA is the mostly studied. In addition, ethylene promotes cell death while JA has a protective role upon O3 exposure. The role of SA is more complicated; depending on the genetic background it can have either cell death promoting or protecting roles. Hence, a clean system to deliver apoplastic ROS is required to study the role of ROS apart from con-current activation of other signaling pathways. Arabidopsis thaliana offer a convenient system to study apoplastic ROS signaling due to the availability of hormone signaling or biosynthesis mutants including the JA receptor mutant coi1-16 (CORONATINE INSENSITIVE1), the essential ethylene signaling mutant ein2 (ETHYLENE INSENSITIVE2), the SA biosynthesis mutant sid2 (SALICYLIC ACID INDUCTION DEFICIENT2 also known as ISOCHORISMATE SYNTHASE1), and essential regulators in SA/JA/ethylene-induced defense response triple mutant tga2 tga5 tga6 (Clade II TGA transcription factors). Here we used a combination of transcriptome analysis, cell death assays and mutant analysis to systematically quantified the contribution of hormone signaling in relation to apoplastic ROS signaling, identified transcription factors (TFs) involved in ROS regulation and dissected the components involved in defense hormones associated cell death. Transcriptome profiling of ozone response using two arabidopsis triple mutants coi1-16 ein2 sid2 and tga2 tga5 tga6 related to Jasmonic acid, salicylic acid and ethylene signaling to identify hormone-independant apoplastic ROS signaling
2015-02-10 | E-GEOD-65740 | biostudies-arrayexpress
Project description:Transcriptome analysis of apoplastic reactive oxygen species signaling and dissection of its regulatory pathways
| PRJNA274887 | ENA
Project description:As sessile organism, plants evolved a highly complicated signaling system to cope with unfavorable and fluctuating environmental conditions. Rapid and transient Reactive Oxygen Species (ROS) burst is a common response to both biotic and abiotic stresses. Plants exposed with O3 could trigger extracellular similar ROS production through cell wall peroxidases and NPADPH oxidases, resulting in changes in the gene expression and cell death. Whereas ROS induced cell death is not simply due to its toxicity, rather due to interplay with several other signaling pathways, such as salicylic acid (SA), jasmonic acid (JA) and ethylene signaling pathways. Furthermore, the three hormones have both synergistic and antagonistic interactions, where the suppression of JA signaling by SA is the mostly studied. In addition, ethylene promotes cell death while JA has a protective role upon O3 exposure. The role of SA is more complicated; depending on the genetic background it can have either cell death promoting or protecting roles. Hence, a clean system to deliver apoplastic ROS is required to study the role of ROS apart from con-current activation of other signaling pathways. Arabidopsis thaliana offer a convenient system to study apoplastic ROS signaling due to the availability of hormone signaling or biosynthesis mutants including the JA receptor mutant coi1-16 (CORONATINE INSENSITIVE1), the essential ethylene signaling mutant ein2 (ETHYLENE INSENSITIVE2), the SA biosynthesis mutant sid2 (SALICYLIC ACID INDUCTION DEFICIENT2 also known as ISOCHORISMATE SYNTHASE1), and essential regulators in SA/JA/ethylene-induced defense response triple mutant tga2 tga5 tga6 (Clade II TGA transcription factors). Here we used a combination of transcriptome analysis, cell death assays and mutant analysis to systematically quantified the contribution of hormone signaling in relation to apoplastic ROS signaling, identified transcription factors (TFs) involved in ROS regulation and dissected the components involved in defense hormones associated cell death.
2015-02-10 | GSE65740 | GEO
Project description:The rapid production of reactive oxygen species (ROS) is a key signaling output in plant immunity. In the angiosperm model species, Arabidopsis thaliana (hereafter Arabidopsis), recognition of non- or altered-self elicitor patterns by cell-surface immune receptors activates the receptor-like cytoplasmic kinases (RLCKs) of the AVRPPHB SUSCEPTIBLE 1 (PBS1)-like (PBL) family, particularly BOTRYTIS-INDUCED KINASE1 (BIK1)1–3. BIK1/PBLs in turn phosphorylate the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase RESPIRATORY BURST OXIDASE HOMOLOG D (RBOHD) to induce apoplastic ROS production4,5. PBL and RBOH functions in plant immunity have been extensively characterized in flowering plants. Much less is known about the conservation of pattern-triggered ROS signaling pathways in non-flowering plants. In this study, we show that, in the liverwort Marchantia polymorpha (hereafter Marchantia), single members of RBOH and PBL families, namely MpRBOH1 and MpPBLa, are required for chitin-induced ROS production. MpPBLa directly interacts with and phosphorylates MpRBOH1 at specific, conserved sites within its cytosolic N-terminus and this phosphorylation is essential for chitin-induced MpRBOH1-mediated ROS production. Collectively, our work reveals the functional conservation of the PBL-RBOH module that controls pattern-triggered ROS production in land plants.
2023-02-06 | PXD038639 | Pride
Project description:The formation of Reactive oxygen species (ROS) has been detected in all cellular departments and even in apoplastic space of plants. As multifaceted molecule, ROS are known to accumulate in response to various stresses, and ROS burst accompanied with transcriptomic reprogramming leading to defense response or programmed cell death. Acute ozone exposure has been used as a noninvasive tool to study ROS burst induced defense response and cell death for a long time. Moreover the variation of ozone sensitivity in different Arabidopsis accessions highlights the flexibility of complex genetic architecture to adapt to specific stresses. In this study, we combine classic Quantitative Trait Loci (QTL) mapping and RNA-seq to identify the cause QTLs and potential gene candidates in response to ozone. RNA sequencing was performed on both control and ozone treated 3 weeks old accessions C24 (ozone tolerant), Te (ozone sensitive) and on a RIL line CT101 (a hypersensitive line of RIL population from reciprocal cross between C24 and Te), in triplicate. We identified 69 potential genes candidates inside the QTL regions and about 200 potential genes outside QTL region in response to ozone by comparing control to treatment within same genotype or comparing control between genotypes. Transcriptome profiling of ozone response using two arabidopsis accessions C24 and Te with different ozone sensitivity
2014-09-19 | E-GEOD-61542 | biostudies-arrayexpress
Project description:Root Meristem Growth Factor 1 (RGF1) controls root meristem size through reactive oxygen species (ROS) signaling
2020-04-15 | E-GEOD-108730 | ExpressionAtlas
Project description:Disruption of circadian clocks exacerbates various diseases, in part likely due to impaired stress resistance. It is unclear how nearly lethal stresses affect circadian clocks. We found that near-lethal doses of reactive oxygen species (ROS)-induced critical oxidative stress (cOS) at the branch point of life and death resets circadian clocks, synergistically evoking protective responses for cell survival. The cOS-triggered clock resetting and pro-survival responses are mediated by transcription factor, central clock-regulatory BMAL1 and heat shock stress-responsive (HSR) HSF1. Casein kinase II (CK2) M-bM-^@M-^Smediated phosphorylation regulates dimerization and function of BMAL1 and HSF1 to control the cOS-evoked responses. The core cOS-responsive transcriptome includes CK2-orchestrated crosstalk between the circadian, HSR, NFM-NM-:B-mediated anti-apoptotic, and Nrf2-mediated anti-oxidant pathways. This novel circadian-adaptive signaling system likely plays fundamental protective roles in ROS-inducible disorders, various diseases, and death. Gene expression was measured 4h, 20h and 32h after treatment with 5 mM H2O2 for 10 min.
2013-11-09 | E-GEOD-47955 | biostudies-arrayexpress
Project description:Weather extremes are increasing worldwide frequently exposing plants to transient flooding. When floodwaters recede, plants have to cope with increased light intensity and elevated oxygen that favor excessive formation of reactive oxygen species (ROS). We report
a novel molecular mechanism that helps Arabidopsis leaves cope with reoxygenation in the light that reveals a central role of the alternative electron tranport in mitochodria in cellular ROS management that is beneficial for photosynthetic recovery and provides tolerance to reoxygenation stress.
2022-12-02 | PXD032119 | JPOST Repository
Project description:The formation of Reactive oxygen species (ROS) has been detected in all cellular departments and even in apoplastic space of plants. As multifaceted molecule, ROS are known to accumulate in response to various stresses, and ROS burst accompanied with transcriptomic reprogramming leading to defense response or programmed cell death. Acute ozone exposure has been used as a noninvasive tool to study ROS burst induced defense response and cell death for a long time. Moreover the variation of ozone sensitivity in different Arabidopsis accessions highlights the flexibility of complex genetic architecture to adapt to specific stresses. In this study, we combine classic Quantitative Trait Loci (QTL) mapping and RNA-seq to identify the cause QTLs and potential gene candidates in response to ozone. RNA sequencing was performed on both control and ozone treated 3 weeks old accessions C24 (ozone tolerant), Te (ozone sensitive) and on a RIL line CT101 (a hypersensitive line of RIL population from reciprocal cross between C24 and Te), in triplicate. We identified 69 potential genes candidates inside the QTL regions and about 200 potential genes outside QTL region in response to ozone by comparing control to treatment within same genotype or comparing control between genotypes.
2014-09-19 | GSE61542 | GEO