Role of NPR1 in SA mediated transcription
Ontology highlight
ABSTRACT:
ORGANISM(S): Arabidopsis thaliana
PROVIDER: GSE51626 | GEO | 2013/12/24
SECONDARY ACCESSION(S): PRJNA224110
REPOSITORIES: GEO
Similar Datasets
Project description:Affymetrix expression analysis was used to validate the role of NPR1 in SA mediated transcription. The RNA of col-0 and npr1-1 mutant were isolated after 24hr water and SA treatment.The ATH1 gene chip was used for expression analysis.
2013-12-24 | E-GEOD-51626 | biostudies-arrayexpress
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
Project description:Salicylic acid (SA) and ethylene (ET) are two important plant hormones that regulate numerous plant growth, development, and stress response processes. Previous studies have suggested functional interplay of SA and ET in defense response, but precisely how these two hormones co-regulate plant growth and development processes remains unclear. The present findings reveal an antagonism between SA and ET in apical hook formation, a process that ensures successful soil emergence of dicotyledonous etiolated seedlings. Exogenous SA inhibited the ET-induced expression of HOOKLESS1 (HLS1) in a manner dependent on ETHYLENE INSENSITIVE3 (EIN3)/EIN3-LIKE1 (EIL1), the core transcription factors in the ET signaling pathway. We found that SA-activated NONEXPRESSER OF PR GENES1 (NPR1) physically interacted with EIN3 and interfered with the direct binding of EIN3 to target gene promoters, including the HLS1 promoter. Transcriptomic analysis further revealed that NPR1 and EIN3/EIL1 coordinately regulated subsets of genes that mediate plant growth and stress responses, suggesting that the interaction between NPR1 and EIN3/EIL1 might be an important mechanism for integrating the SA and ET signaling pathways in multiple physiological processes. Taken together, our findings shed light on the molecular mechanism underlying SA regulation of apical hook formation as well as the antagonism between SA and ET in early seedling establishment and possibly other physiological processes.
2020-08-20 | GSE137212 | GEO
Project description:Genome-wide direct targets of Arabidopsis NPR1 and HAC1 were identified by chromain immunoprecipitation followed by sequencing (ChIP-seq). For the study, we used Arabidopsis expressing NPR1:GFP or HAC1:mCherry under native NPR1 or HAC1 promoter, respectively. To identify direct targets both under salicylic acid-treated and untreated conditions, we performed ChIP-seq by using 2,6-dichloroisonicotinc acid (INA; synthetic SA analog)-treated and untreated NPR1:GFP or HAC1:mCherry transgenic Arabidopsis plants.
2023-12-25 | GSE211047 | GEO
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
Project description:The Arabidopsis Pathoarray 464_001 (GPL3638) was used to compare response of Col-0, pad4-1 (Zhou et al., 1998; Jirage et al., 1999) and sid2-2 (Wildermuth et al., 2001) to Pseudomonas syringae pv. tomato DC3000 hrcC mutant. SA production is drastically reduced in sid2 mutants. PAD4 is required for SA-mediated responses. The results suggested that the SA increase triggered by MAMPs is one major component in the MAMPs-triggered signaling mechanism. Keywords: Responses of Arabidopsis to Pseudomonas syringae pv. tomato DC3000 hrcC mutant
2007-07-14 | GSE8273 | GEO
Project description:Zhou2015 - Circadian clock with immune
regulator NPR1
Arabidopsis clock model modified from
P2012 (Pokhilko et al., 2013 -
BIOMD0000000445)
model to include the master immune regulator NPR1 coupling to LHY,
TOC1 and PRR7.
Triggers: The Global Quantities contain triggers that allow
one to change coupling settings, Salicyclic acid (SA) treatment and
npr1 mutants.
LHY_on: true->NPR1 couples to LHY
PRR7_on: true->NPR1 couples to PRR7
WT: true->WT plants, false->npr1 mutant plants
SA: true->SA treated plants, false->no treatment
This model has L=1, i.e. operates only under constant light
conditions and is not aiming to make preditions under diurnal
conditions. Due to period overshoot only time points after 28h are
relevant.
This model is described in the article:
Redox rhythm reinforces the
circadian clock to gate immune response.
Zhou M, Wang W, Karapetyan S, Mwimba
M, Marqués J, Buchler NE, Dong X.
Nature 2015 Jun;
Abstract:
Recent studies have shown that in addition to the
transcriptional circadian clock, many organisms, including
Arabidopsis, have a circadian redox rhythm driven by the
organism's metabolic activities. It has been hypothesized that
the redox rhythm is linked to the circadian clock, but the
mechanism and the biological significance of this link have
only begun to be investigated. Here we report that the master
immune regulator NPR1 (non-expressor of pathogenesis-related
gene 1) of Arabidopsis is a sensor of the plant's redox state
and regulates transcription of core circadian clock genes even
in the absence of pathogen challenge. Surprisingly, acute
perturbation in the redox status triggered by the immune signal
salicylic acid does not compromise the circadian clock but
rather leads to its reinforcement. Mathematical modelling and
subsequent experiments show that NPR1 reinforces the circadian
clock without changing the period by regulating both the
morning and the evening clock genes. This balanced network
architecture helps plants gate their immune responses towards
the morning and minimize costs on growth at night. Our study
demonstrates how a sensitive redox rhythm interacts with a
robust circadian clock to ensure proper responsiveness to
environmental stimuli without compromising fitness of the
organism.
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BIOMD0000000577.
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2015-07-10 | BIOMD0000000577 | BioModels
Project description:Salicylic acid (SA) is a plant defense hormone required for immunity. Arabidopsis NPR1 and NPR3/NPR4 were previously shown to bind SA and proposed as SA receptors. However, unlike NPR1, loss of NPR3/NPR4 does not block SA-induced defense gene expression. Here we report that NPR3/NPR4 function as transcriptional repressors and SA inhibits their activities to promote the expression of key immune regulators. npr4-4D, a newly identified gain-of-function allele that renders NPR4 unable to bind SA, constitutively represses SA-induced immune responses. In contrast, the equivalent mutation in NPR1 abolishes its function in promoting SA-induced defense gene expression. Further analysis revealed that npr4-4D and npr1-1 have additive effect on blocking SA-induced defense gene expression, suggesting that NPR4 and NPR1 function in parallel to regulate SA-induced immune responses. Our study reveals the molecular functions of SA receptors NPR3/NPR4 and uncovers a brand new mechanism of SA perception.
2018-06-08 | GSE110702 | GEO
Project description:To investigate the mechanism of NPR1 regulating vascular function, we established NPR1 knockout heterozygous mice by CRISPR-Cas9. We performed high-throughput RNA sequencing to analyse the transcriptom of the aorta of NPR1 knocout heterogeneous mice.
2022-10-14 | GSE215215 | GEO
Project description:We report novel function of NPR1 coactivator that regulates cold acclimation by promoting cold-induced gene expression.
2018-08-31 | GSE101483 | GEO