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Arabidopsis thaliana

ABSTRACT: JAZ proteins enhance the expression of SA/NPR1-responsive genes.

PROVIDER: PRJDB3560 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	DRR031018.fastq.gz	Fastqsanger.gz
	DRR031019.fastq.gz	Fastqsanger.gz
	DRR031020.fastq.gz	Fastqsanger.gz
	DRR031021.fastq.gz	Fastqsanger.gz
	DRR031022.fastq.gz	Fastqsanger.gz

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Arabidopsis thaliana

Project description:SA suppresses JA-responsive gene expression through the transcription cofactor NPR1.

| PRJDB3559 | ENA

Salicylic acid-induced gene expression in wild-type Col-0 and mutant upl1, upl5, and npr1-1 Arabidopsis thaliana plants

Project description:The plant immune hormone salicylic acid (SA) modulates transcriptional reprogramming via controlling the master transcriptional coactivator, NPR1. Here we examined the role of HECT-type ubiquitin ligases, UPL1 and UPL5, in SA/NPR1-dependent transcriptional control. We showed that UPL1 and UPL5 are essential regulators of SA-responsive genes, and regulate SA-induced transcriptional reprogramming in a NPR1-dependent manner. Four-week old Arabidopsis thaliana plants of wild-type Col-0, mutant upl1, mutant upl5, and mutant npr1-1 genotypes were germinated on soil in 100% relative humidity. Plants were continuously grown in an environmental chamber with 16/8 hour day/night light regime (120 mol m-2 s-1 light intensity), 21/18 degrees celcius day/night cycle and 65% relative humidity. 4-week-old plants were sprayed with water or 0.5 mM SA until all leaves were thoroughly covered with fine droplets, samples were collected after 24 hours treatment. In total two independent biological repeats were collected.

2021-10-05 | E-MTAB-10963 | biostudies-arrayexpress

JASMONATE-ZIM DOMAIN proteins engage Polycomb chromatin modifiers to modulate Jasmonate signaling in Arabidopsis [ChIP-Seq]

Project description:JASMONATE-ZIM DOMAIN (JAZ) proteins are key regulators in the JA signaling pathway and function to repress the expression of JA-responsive genes. We found that JAZ proteins directly interact with several chromatin-associated Polycomb proteins to mediate repressive chromatin modifications at part of JA-responsive genes and thus their transcriptional repression in Arabidopsis.

2023-07-19 | GSE167636 | GEO

JASMONATE-ZIM DOMAIN proteins engage Polycomb chromatin modifiers to modulate Jasmonate signaling in Arabidopsis [RNA-Seq]

2023-07-19 | GSE167633 | GEO

Arabidopsis thaliana

Project description:Role of NPR1 in SA mediated transcription

| PRJNA224110 | ENA

Novel JAZ co-operativity and unexpected JA dynamics underpin Arabidopsis defence responses to Pseudomonas syringae infection

Project description:Pathogens target phytohormone signalling pathways to promote disease. Plants deploy salicylic acid (SA) mediated defences against biotrophs. Pathogens antagonise SA immunity by activating jasmonate signalling, e.g. Pseudomonas syringae pv. tomato DC3000 produces coronatine (COR), a jasmonate (JA) mimic. This study found unexpected dynamics between SA, JA and COR and co-operation between JAZ jasmonate repressor proteins during DC3000 infection. JA did not accumulate until late in the infection process and was higher in leaves challenged with coronatine deficient P. syringae or in the more resistant JA receptor mutant coi1. JAZ regulation was complex and coronatine alone was insufficient to sustainably induce JAZs.

2015-08-28 | GSE72461 | GEO

Arabidopsis thaliana

Project description:NINJA connects JAZ proteins to the co-repressor TOPLESS

| PRJNA120319 | ENA

A pair of NUCLEAR FACTOR Y transcription factors act as positive regulators in jasmonate signaling and disease resistance in Arabidopsis

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.

2024-07-15 | GSE247054 | GEO

A pair of NUCLEAR FACTOR Y transcription factors act as positive regulators in jasmonate signaling and disease resistance in Arabidopsis

2024-07-15 | GSE247053 | GEO

Oxicam-type nonsteroidal anti-inflammatory drugs inhibit NPR1-mediated salicylic acid pathway

Project description:Nonsteroidal anti-inflammatory drugs (NSAIDs), including salicylic acid (SA), target mammalian cyclooxygenases. In plants, SA is a defense hormone that regulates NON-EXPRESSOR OF PATHOGENESIS RELATED GENES 1 (NPR1), the master transcriptional regulator of immunity-related genes. We identify that the oxicam-type NSAIDs tenoxicam (TNX), meloxicam, and piroxicam, but not other types of NSAIDs, exhibit an inhibitory effect on immunity to bacteria and SA-dependent plant immune response. TNX treatment decreases NPR1 levels, independently from the proposed SA receptors NPR3 and NPR4. Instead, TNX induces oxidation of cytosolic redox status, which is also affected by SA and regulates NPR1 homeostasis. A cysteine labeling assay reveals that cysteine residues in NPR1 can be oxidized in vitro, leading to disulfide-bridged oligomerization of NPR1, but not in vivo regardless of SA or TNX treatment. Therefore, this study indicates that oxicam inhibits NPR1-mediated SA signaling without affecting the redox status of NPR1.

2021-11-09 | GSE154593 | GEO

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