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Arabidopsis thaliana

ABSTRACT: Alternaria brassicicola infection regulates miRNAs in Arabidopsis thaliana [mRNA]

PROVIDER: PRJNA326102 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3680100.fastq.gz	Fastqsanger.gz
	SRR3680101.fastq.gz	Fastqsanger.gz
	SRR3680102.fastq.gz	Fastqsanger.gz
	SRR3680094.fastq.gz	Fastqsanger.gz
	SRR3680095.fastq.gz	Fastqsanger.gz

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Project description:Alternaria brassicicola infection regulates miRNAs in Arabidopsis thaliana [sRNA]

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Alternaria brassicicola infection regulates miRNAs in Arabidopsis thaliana [sRNA]

Project description:Plant microRNAs (miRNAs) have been implicated in plant immunity. These mainly focusing Arabidopsis thaliana threatened by (hemi-)biotrophic pathogens such as the bacterial pathogen Pseudomonas syringae. Here, we show that the Arabidopsis miRNA pathway is important for defense responses against the necrotrophic fungus Alternaria brassicicola. The miRNA pathway mutant ago1 exhibits an exaggerated response when treated with A. brassicicola, proposing that AGO1 is positive regulator. We found a subset of Arabidopsis miRNAs that quickly change their expression and their abundance in AGO1 complexes in plants exposed to A. brassicicola. The miRNAs responding to pathogen treatment are mainly targeting genes encoding metabolic enzymes, proteins involved protein degradation or transposons. In case of miR163, A. brassicicola infection results in increased levels of miRNA precursors and preferential accumulation of an unspliced form of pri-miR163, suggesting that A. brassicicola infection changes the transcriptional and post-regulation of pri-miRNAs. miR163 acts as a negative regulator of plant defense because mir163 mutants are more resistant when treated with A. brassicicola. Taken together, our results reveal the existence of positively and negatively acting Arabidopsis miRNA modulating the defense responses against A. brassicicola and highlight the importance of host miRNAs in the interaction between plants and necrotrophic pathogens.

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Arabidopsis thaliana gene expression upon exposure to nanoparticles (NPs), biotic and abiotic stresses, or NPs plus ABA phytohormone, PART 1

Project description:Here we provide a set of 16 comparable transcriptome measures to monitor early changes in gene expression upon NP exposure. We evaluated A. thaliana response to 8 different types of NPs (metallic, carbonaceous and ranging from 10 to 80 nm) in comparison to biotic and abiotic stress inducers that represent most common environmental challenges for plants. Biotic stress was induced by infection with a necrotizing fungus (Alternaria brassicicola) or a hemibiotrophic bacterium (Pseudomonas syringae). Abiotic stresses induced by hypersaline conditions, drought and mechanical wounding were assayed in our plant growth model. The effect of abscisic acid (ABA), the most studied stress-responsive phytohormone which mediates stomatal closure and other reponses to drought and osmotic stress (ref), was also tested in the gene expression and phenotypes of NP-exposed plants. PART 1: Alternaria brassicicola (Abr), Pseudomonas syringae (Pst), saline stress (NaC), drought (drou), wounding (wou), 10nm TiO2 NPs (TiO2 10), 10nm AgNPs (Ag 10), bulk TiO2 (TiO), bulk AgNO3 (NO), Carbon Nanotubes NPs plus ABA (CNTs+). susana.garcias@ehu.es<a href=susana.garcias@ehu.es>additional contact details for submitter</a>

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Dual-transcritome analysis of germinating Arabidopsis seeds in response to necrotrophic fungus Alternaria brassicicola

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Project description:We analyzed transcriptome changes from germinating cyp79B2 cyp79B3, qko, and pad3 mutant Arabidopsis seeds. Here were used mutant lines in Col-0 genetic background: a cyp79B2 cyp79B3 double mutant defective in indolic glucosinolate (cyp79B2/B3), a cyp79B2 cyp79B3 myb28 myb29 quadruple mutant defective in indolic and aliphatic glucosinolates (qko), and a camalexin deficient mutant (pad3). Differentially expressed genes were identified at 3, 6 and 10 days after sowing from both the mutant line seeds and from Alternaria brassicicola when inoculated seeds were analyzed.

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