Ontology highlight
ABSTRACT:
PROVIDER: PRJNA813366 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18250421.fastq.gz | Fastqsanger.gz | |||
| SRR18250422.fastq.gz | Fastqsanger.gz | |||
| SRR18250423.fastq.gz | Fastqsanger.gz | |||
| SRR18250424.fastq.gz | Fastqsanger.gz | |||
| SRR18250425.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
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Project description:The Arabidopsis rosette core can display full resistance against Botrytis cinerea. To reveal potential players in this resistance, the transcriptome of the Arabidopsis rosette core was determined.
2019-04-09 | GSE129452 | GEO
Project description:The Arabidopsis thaliana mutant wrky33 is highly susceptible to the necrotrophic fungus Botrytis cinerea. We identified by ChIP-seq >1680 high-confidence WRKY33 binding sites associated with 1576 genes within the Arabidopsis genome, with all of them being dependent on rapid activation of WRKY33 expression by Botrytis cinerea strain 2100. Genome-wide transcriptional analysis defined 318 genes as direct functional targets at 14 h post inoculation. Comparison between resistant wild-type Columbia-0 and susceptible wrky33 mutant plants revealed that expression of 75% of all WRKY33 regulated targets were down-regulated upon infection, indicating that WRKY33 predominately acts as a repressor. However, WRKY33 appears to possess dual functionality acting either as a repressor or as an activator in a promoter-context dependent manner. Our genome-wide analysis confirmed known WRKY33 targets involved in ethylene and jasmonic acid hormone signaling and phytoalexin biosynthesis, but also uncovered a previously unknown role of abscisic acid (ABA) biosynthesis in the complex regulatory circuitry affecting resistance towards Botrytis. Analysis of transgenic plants expressing WRKY33-HA under its native promoter post inoculation with spores of Botrytis cinerea 2100
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Project description:To investigate NUP62 in the regulation of plant defense against Botrytis cinerea , we performed gene expression profiling analysis using data obtained from RNA-seq of nup62 mutant and WT arabidopsis with or without Botrytis cinerea infection.
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Project description:The plant hormone jasmonate (JA) regulates plant growth and immunity by orchestrating a genome-wide transcriptional reprogramming. In the resting stage, JASMONATE-ZIM DOMAIN (JAZ) proteins act as main repressors to regulate the expression of JA-responsive genes in the JA signaling pathway. However, the mechanisms underlying de-repression of JA-responsive genes in response to JA treatment remain elusive. Here, we report two nuclear factor Y transcription factors NF- YB2 and NF-YB3 (thereafter YB2 and YB3) play key roles in such de-repression in Arabidopsis. YB2 and YB3 function redundantly and positively regulate plant resistance against necrotrophic pathogen Botrytis cinerea ， which are specially required for transcriptional activation of a set of JA-responsive genes following inoculation. Furthermore, YB2 and YB3 modulated their expression through direct occupancy and interaction with histone demethylase Ref6 to remove repressive histone modifications. Moreover, YB2 and YB3 physically interacted with JAZ repressorsand negatively modulated their abundance, which in turn attenuated the inhibition of JAZ proteins on the transcription of JA- responsive genes, thereby activating JA response and promoting disease resistance. Overall, our study reveals the positive regulator of YB2 and YB3 in JA signaling by positively regulating transcription of JA-responsive genes and negatively modulating the abundance of JAZ proteins.
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Project description:Arabidopsis overexpressing ERF96 are more resistant against necrotrophic pathogen such as Botrytis cinerea. ERF96 is a member of the AP2/ERF superfamily of transcription factor. We used Microarray to determine which gene expressions are up-regulated due to an accumulation of ERF96 and to identify the putative direct target of this transcription factor.
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Project description:The Arabidopsis thaliana mutant wrky33 is highly susceptible to the necrotrophic fungus Botrytis cinerea. We identified by ChIP-seq >1680 high-confidence WRKY33 binding sites associated with 1576 genes within the Arabidopsis genome, with all of them being dependent on rapid activation of WRKY33 expression by Botrytis cinerea strain 2100. Genome-wide transcriptional analysis defined 318 genes as direct functional targets at 14 h post inoculation. Comparison between resistant wild-type Columbia-0 and susceptible wrky33 mutant plants revealed that expression of 75% of all WRKY33 regulated targets were down-regulated upon infection, indicating that WRKY33 predominately acts as a repressor. However, WRKY33 appears to possess dual functionality acting either as a repressor or as an activator in a promoter-context dependent manner. Our genome-wide analysis confirmed known WRKY33 targets involved in ethylene and jasmonic acid hormone signaling and phytoalexin biosynthesis, but also uncovered a previously unknown role of abscisic acid (ABA) biosynthesis in the complex regulatory circuitry affecting resistance towards Botrytis.
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Project description:To screen Botrytis genes activated in infection process, we performed gene expression profiling analysis using data obtained from RNA-seq of Botrytis cinerea cultured in vitro or infecting Arabidopsis leaves.
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Project description:The Arabidopsis thaliana mutant wrky33 is highly susceptible to the necrotrophic fungus Botrytis cinerea. Comparing the expression profiles of B. cinerea-infected wrky33 and WT plants we identified 2765 differentially expressed genes dependent on WRKY33, of which 1675 were up-regulated in the mutant (termed WRKY33-repressed genes) and 1090 were down-regulated in the mutant. Combined with ChIP-seq data 318 genes were identified as direct functional targets of WRKY33 at 14 h post inoculation with spores of Botrytis cinerea 2100. Comparison of altered gene expression in Arabidopsis WT and wrky33 mutant plants 14 hours post inoculation with Botrytis cinerea 2100.
2015-06-15 | E-GEOD-66290 | biostudies-arrayexpress
Project description:Current protection strategies against the fungal pathogen Botrytis cinerea rely on a combination of conventional fungicides and host genetic resistance. Defence elicitors can stimulate plant defence mechanisms through a phenomenon known as priming. Priming results on a faster and/or stronger expression of resistance upon pathogen attack. This work aims to study priming of a commercial formulation of the elicitor Chitosan. Treatments with Chitosan result in induced resistance in solanaceous and brassicaceous plants. Large-scale transcriptomic analysis in this study revealed that Chitosan primes gene expression at early time-points after infection. Four conditions were analysed using microarrays: (i) water-treated and non-infected plants (Water + Mock); (ii) Chitosan-treated and non-infected plants (Chitosan + Mock); (iii) water-treated and B. cinerea-infected plants (Water + B. cinerea); (iv) Chitosan-treated and B. cinerea-infected plants (Chitosan + B. cinerea). Inoculations were performed four days after treatment with Chitosan, and leaf discs from four independent plants (biological replicates) per treatment were sampled at 6 h, 9 h and 12 h post-inoculation (hpi) with water mock or B. cinerea spores.
2020-07-01 | E-MTAB-8868 | biostudies-arrayexpress
Project description:The plant hormone jasmonate (JA) regulates plant growth and immunity by orchestrating a genome-wide transcriptional reprogramming. In the resting stage, JASMONATE-ZIM DOMAIN (JAZ) proteins act as main repressors to regulate the expression of JA-responsive genes in the JA signaling pathway. However, the mechanisms underlying de-repression of JA-responsive genes in response to JA treatment remain elusive. Here, we report two nuclear factor Y transcription factors NF- YB2 and NF-YB3 (thereafter YB2 and YB3) play key roles in such de-repression in Arabidopsis. YB2 and YB3 function redundantly and positively regulate plant resistance against necrotrophic pathogen Botrytis cinerea ， which are specially required for transcriptional activation of a set of JA-responsive genes following inoculation. Furthermore, YB2 and YB3 modulated their expression through direct occupancy and interaction with histone demethylase Ref6 to remove repressive histone modifications. Moreover, YB2 and YB3 physically interacted with JAZ repressorsand negatively modulated their abundance, which in turn attenuated the inhibition of JAZ proteins on the transcription of JA- responsive genes, thereby activating JA response and promoting disease resistance. Overall, our study reveals the positive regulator of YB2 and YB3 in JA signaling by positively regulating transcription of JA-responsive genes and negatively modulating the abundance of JAZ proteins.
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