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Arabidopsis thaliana

ABSTRACT: Gene expression profile during wound-induced callus formation in Arabidopsis thaliana

PROVIDER: PRJNA394215 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5826950.fastq.gz	Fastqsanger.gz
	SRR5826951.fastq.gz	Fastqsanger.gz
	SRR5826942.fastq.gz	Fastqsanger.gz
	SRR5826952.fastq.gz	Fastqsanger.gz
	SRR5826943.fastq.gz	Fastqsanger.gz

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Gene expression profile during wound-induced callus formation in Arabidopsis thaliana

Project description:Wounding is a primary trigger of organ regeneration but how wound stress reactivates cell proliferation and promotes cellular reprogramming remains elusive. In this study we combined the transcriptome analysis with quantitative hormonal analysis to investigate how wounding induces callus formation in Arabidopsis thaliana. Our time-course RNA-seq analysis revealed that wounding induces dynamic transcriptional changes that can be categorized into five clusters with distinct temporal patterns. Gene ontology analyses uncovered that wounding modifies the expression of hormone biosynthesis and response genes, and quantitative analysis of endogenous plant hormones revealed accumulation of cytokinin prior to callus formation. Mutants defective in cytokinin synthesis and signalling display reduced efficiency in callus formation, indicating that de novo synthesis of cytokinin has major contribution in wound-induced callus formation. We further demonstrate that type-A ARABIDOPSIS RESPONSE REGULATOR (ARR)-mediated cytokinin signalling regulates the expression of CYCLIN D3;1 (CYCD3;1) and mutations in CYCD3;1 and its homologs CYCD3;2-3 cause defects in callus formation. Our transcriptome data, in addition, showed that wounding activates multiple developmental regulators, and we found novel roles of ETHYLENE RESPONSE FACTOR 115 (ERF115) and PLETHORA3 (PLT3), PLT5, PLT7 in wound-induced callus formation. Together, this study provides novel mechanistic insights into how wounding reactivates cell proliferation during callus formation.

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Project description:Transcriptional profiling of cotyledon transcriptomics at the seedling stage (6 d) by comparison of wild-type vs. cotyledon-less laterne (= pid enp) homozygous mutant. The goal was to determine the transcriptomic profile of a cotyledon. The experiment took advantage of the endogenously caused lack of cotyledons instead of dissecting these organs, which would cause wound-induced expression.This was achieved by comparing seedlings of the Arabidopsis thaliana pid enp double mutant, which is incapable to generate cotyledons. This is caused by the loss of apical cell polarisation of the auxin efflux carrier PIN1 in epidermal cells during embryogenesis.

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Project description:The goal of this project is to compare the primary metabolite profile in different tissue types of the model plant Arabidopsis thaliana. Specifically, plants were grown hydroponically under the long-day (16hr light/day) condition at 21C. Tissue samples, including leaves, inflorescences, and roots were harvest 4 1/2 weeks post sowing. Untargeted primary metabolites profiling was carried out using GCTOF.

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WIND1 orchestrates wound-induced callus formation, vascular reconnection and defense response in Arabidopsis

Project description:Wounding triggers de novo organogenesis, vascular reconnection and defense response but how wound stress evokes such a diverse array of physiological responses remains unknown. We previously identified an AP2/ERF transcription factor, WOUND INDUCED DEDIFFERENTIATION1 (WIND1), as a key regulator of wound-induced cellular reprogramming in Arabidopsis. To understand how WIND1 promotes downstream events, we performed time-course transcriptome analyses after WIND1 induction. We observed a significant overlap between WIND1-induced genes and genes implicated in cellular reprogramming, vascular formation and pathogen response. We demonstrated that WIND1 induces several reprogramming genes to promote callus formation at wound sites. We, in addition, showed that WIND1 promotes tracheary element formation, vascular reconnection and flagellin-triggered defense responses. These results indicate that WIND1 functions as a master regulator of wound-induced responses by promoting dynamic transcriptional alterations. This study provides deeper mechanistic insights into how plants control multiple physiological responses after wounding.

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