Arabidopsis thaliana
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB10143 | ENA |
REPOSITORIES: ENA
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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:SA suppresses JA-responsive gene expression through the transcription cofactor NPR1.
| PRJDB3559 | ENA
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:Role of NPR1 in SA mediated transcription
| PRJNA224110 | ENA
Project description:RNA-Seq timeseries of Arabidopsis Mock, JA or SA treated
| PRJNA224133 | ENA
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.
This model is hosted on
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and identified by:
BIOMD0000000577.
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2015-07-10 | BIOMD0000000577 | BioModels
Project description:NPR1 is a central positive regulator of salicylic-acid (SA)-mediated defense signaling in Arabidopsis. Here, we report characterization of OsNPR1, an Oryzae sativa (rice) ortholog of NPR1, focusing on its role in blast disease resistance and identification of OsNPR1-regulated genes followed by their comparison with NPR1-regulated genes in Arabidopsis. Blast resistance tests using OsNPR1–knockdown and –overexpressing rice lines indicated that OsNPR1 plays an essential role in benzothiadiazole-induced blast resistance. Genome-wide transcript profiling using OsNPR1–knockdown lines revealed that 358 genes out of 1,228 BTH-upregulated genes and 724 genes out of 1,069 BTH-downregulated genes were OsNPR1 dependent with respect to their BTH responsiveness, indicating that OsNPR1 plays a major role in the downregulation. Inspection of OsNPR1-dependent genes revealed that many genes involved in photosynthesis and chloroplastic translation and transcription were downregulated by BTH in an OsNPR1 dependent manner, indicating that photosynthesis and chloroplast activities is coordinately suppressed by OsNPR1 in response to BTH-induced activation of SA-signaling pathway. ABA-responsive genes were also OsNPR1-dependently downregulated, suggesting antagonistic interaction of SA signaling on ABA signaling. None of 11 BTH-upregulated genes for WRKY transcription factors was OsNPR1 dependent, whereas most of those are NPR1-dependently upregulated in Arabidopsis, indicating that the role of OsNPR1 is distinct from that of NPR1 in Arabidopsis. We discuss the significance of OsNPR1-regulated gene expression in SA-regulated defense program and the role of OsNPR1 in rice SA-signaling pathway that is branched to OsNPR1- and rice WRKY45-dependent sub-pathways. mock-treated wild-type (Nipponbare) rice, benzothiadiazole (BTH)-treated wild-type rice, mock-treated WRKY45-knockdown rice (2 lines) and BTH-treated WRKY45-knockdown rice (2 lines) were analyzed in four biological replicates.
2010-12-24 | E-GEOD-16144 | biostudies-arrayexpress
Project description:Expression data of T87 Arabidopsis cultured cells in the presence of ABA, SA, JA, ABA+SA, or ABA+JA for 3hr or 24hr
| PRJNA139101 | ENA
Project description:Activation of plant immunity is associated with dramatic transcriptome reprogramming to prioritise immune responses over normal cellular functions. Changes in gene expression are coordinated by the immune hormone salicylic acid (SA). Here we investigated the involvement of the E4 ubiquitin ligase UBE4/MUSE3 in SA-induced transcriptional reprogramming. We show that loss of UBE4 function results in amplified expression of SA-induced, NPR1-dependent gene expression. Twelve-day old Arabidopsis thaliana seedlings of wild-type Col-0, mutant ube4 (SAIL_713_A12) and mutant npr1-1 genotypes were grown on MS media supplemented with 1X Gamborg vitamins in an environmental chamber with 16/8 hour day/night light regime (120 mol m-2 s-1 light intensity) and 22 degrees Celcius. Seedlings were then transferred to 6-well plates and immersed in 10 ml of 0.5 mM SA or water. After 12 hours seedlings were harvested and for each treatment ~50 seedlings were pooled together into a single biological repeat. In total two independent biological repeats were collected. After harvesting seedlings were briefly dried on tissue and immediately frozen in liquid nitrogen until further analysis.
2019-03-20 | E-MTAB-7369 | biostudies-arrayexpress
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