Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcriptome analysis of apoplastic reactive oxygen species (ROS) signaling and dissection of the roles of WRKY25, WRKY33 and WRKY75 in the transcriptional reprogramming triggered by apoplastic ROS

ABSTRACT: In order to dissect the roles of sequence-specific transcription factors WRKY25, WRKY33 and WRKY75 in apoplastic ROS signaling, a transcriptome profiling of ozone response was done using two arabidopsis mutants: a double mutant wrky25 wrky33 and a single mutant wrky75. The single mutant lines used for transcriptomic analyses were obtained from NASC: wrky25 (SAIL_529_B11) and wrky33 (SALK_006603) were crossed to generate double mutant wrky25 wrky33. T-DNA insertion mutant wrky75-25 (N121525) was obtained from NASC. Three biological replicates, five plants per replicate, treated with 350 ppb ozone for 2 hours, were used for RNA-seq analysis. For each genotype, also non-ozone-treated samples were collected. For the Col-0 control line, an additional fourth replicate with/without ozone was done.

ORGANISM(S): Arabidopsis thaliana

SUBMITTER: Mikael Brosche

PROVIDER: E-GEOD-79855 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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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Transcriptome analysis of apoplastic reactive oxygen species (ROS) signaling and dissection of the roles of WRKY25, WRKY33 and WRKY75 in the transcriptional reprogramming triggered by apoplastic ROS

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