Unknown,Transcriptomics,Genomics,Proteomics

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Thioredoxin DCC1 regulates shoot regeneration through modulating multiple genes expression by RNA-seq analyses in Arabidopsis

ABSTRACT: The capacity of plant regeneration in different ecotypes of Arabidopsis largely varies. However, the mechanism underlying this process remains exclusive. Here, we identified a critical thioredoxin gene DCC1 in determining natural variation for shoot regeneration in Arabidopsis. Functional loss of DCC1 resulted in the repression of shoot regeneration. DCC1 encodes a thioredoxin, which was localized in mitochondria. DCC1 directly interacted with CARBONIC ANHYDRASE 2 (CA2) to regulate the mitochondrial respiratory complex activity and mediate the Reactive Oxygen Species (ROS) level. Defects of DCC1 or CA2 caused the increased ROS level. To understand the regulatory mechanism of DCC1-mediated ROS in shoot regeneration, we analyzed the transcript levels of wild type Col-0 and the mutant dcc1 calli during shoot regeneration by RNA-seq. Three biological repeats of wild type Co-0 and the mutant dcc1 calli were used for RNA sequencing. Total RNAs were isolated from the calli of wild type Col-0 and the mutant dcc1 cultured on shoot-induction medium. The RNA-seq was performed using the Illumina Hiseq 2500. The raw reads were aligned to the genome sequences of TAIR10 using Tophat2 software. The gene expression levels were measured in FPKM, and many critical genes were identified to be involved in shoot regeneration.

INSTRUMENT(S): Illumina HiSeq 2500

ORGANISM(S): Arabidopsis thaliana

SUBMITTER: Hui Liu

PROVIDER: E-MTAB-5236 | 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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Thioredoxin DCC1 regulates shoot regeneration through modulating multiple genes expression by RNA-seq analyses in Arabidopsis

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