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Quantitative trait loci mapping and transcriptome analysis reveal candidate genes regulating the response to ozone in Arabidopsis thaliana

ABSTRACT: 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.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE61542 | GEO | 2014/09/19

SECONDARY ACCESSION(S): PRJNA261430

REPOSITORIES: GEO

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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

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Quantitative trait loci mapping and transcriptome analysis reveal candidate genes regulating the response to ozone in Arabidopsis thaliana

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