Phosphoproteomic analysis of mpk1/2/7/14 treated with mannitol or abscisic acid
Ontology highlight
ABSTRACT:
ORGANISM(S): Arabidopsis Thaliana (mouse-ear Cress)
SUBMITTER: Taishi Umezawa
PROVIDER: PXD045815 | JPOST Repository | Sat Sep 30 00:00:00 BST 2023
REPOSITORIES: jPOST
Similar Datasets
Project description:Stomata open in response to light and close following exposure to abscisic acid (ABA). They regulate gas exchange between plants and atmosphere, allowing plants to adapt to changing environmental conditions. ABA binding to receptors initiates a signaling cascade that involves protein phosphorylation. Here we show that ABA induced phosphorylation of three basic helix-loop-helix (bHLH) transcription factors, called AKSs (ABA-RESPONSIVE KINASE SUBSTRATES; AKS1, AKS2, AKS3), in Arabidopsis guard cells, and that they facilitated stomatal opening through the transcription of genes encoding inwardly-rectifying K+ channels. aks1aks2-1 double mutant plants showed decreases in light-induced stomatal opening, K+ accumulation in response to light, activity of inwardly-rectifying K+ channels, and transcription of genes encoding major inwardly-rectifying K+ channels. Overexpression of POTASSIUM CHANNEL IN ARABIDOPSIS THALIANA 1 (KAT1), which encodes a major inwardly-rectifying K+ channel in guard cells, rescued the phenotype of aks1aks2-1 plants. AKS1 bound directly to the promoter of KAT1, an interaction that was attenuated after ABA-induced phosphorylation. The ABA agonist pyrabactin induced phosphorylation of AKSs. Our results demonstrate that the AKS family of bHLH transcription factors facilitates stomatal opening through transcription of genes encoding inwardly-rectifying K+ channels, and that ABA suppresses the activity of inwardly-rectifying K+ channel activity by triggering the phosphorylation of these transcription factors. To find the affect of AKS1 and AKS2 transcription factors on gene expression, Arabidopsis guard cell protoplasts from wild type and aks1aks2-1 mutant were compared. Three independent experiments were performed.
2013-06-17 | E-GEOD-46574 | biostudies-arrayexpress
Project description:Stomata open in response to light and close following exposure to abscisic acid (ABA). They regulate gas exchange between plants and atmosphere, allowing plants to adapt to changing environmental conditions. ABA binding to receptors initiates a signaling cascade that involves protein phosphorylation. Here we show that ABA induced phosphorylation of three basic helix-loop-helix (bHLH) transcription factors, called AKSs (ABA-RESPONSIVE KINASE SUBSTRATES; AKS1, AKS2, AKS3), in Arabidopsis guard cells, and that they facilitated stomatal opening through the transcription of genes encoding inwardly-rectifying K+ channels. aks1aks2-1 double mutant plants showed decreases in light-induced stomatal opening, K+ accumulation in response to light, activity of inwardly-rectifying K+ channels, and transcription of genes encoding major inwardly-rectifying K+ channels. Overexpression of POTASSIUM CHANNEL IN ARABIDOPSIS THALIANA 1 (KAT1), which encodes a major inwardly-rectifying K+ channel in guard cells, rescued the phenotype of aks1aks2-1 plants. AKS1 bound directly to the promoter of KAT1, an interaction that was attenuated after ABA-induced phosphorylation. The ABA agonist pyrabactin induced phosphorylation of AKSs. Our results demonstrate that the AKS family of bHLH transcription factors facilitates stomatal opening through transcription of genes encoding inwardly-rectifying K+ channels, and that ABA suppresses the activity of inwardly-rectifying K+ channel activity by triggering the phosphorylation of these transcription factors.
2013-06-17 | GSE46574 | GEO
Project description:Stomata open in response to light and close following exposure to abscisic acid (ABA). They regulate gas exchange between plants and atmosphere, allowing plants to adapt to changing environmental conditions. ABA binding to receptors initiates a signaling cascade that involves protein phosphorylation. Here we show that ABA induced phosphorylation of three basic helix-loop-helix (bHLH) transcription factors, called AKSs (ABA-RESPONSIVE KINASE SUBSTRATES; AKS1, AKS2, AKS3), in Arabidopsis guard cells, and that they facilitated stomatal opening through the transcription of genes encoding inwardly-rectifying K+ channels. aks1aks2-1 double mutant plants showed decreases in light-induced stomatal opening, K+ accumulation in response to light, activity of inwardly-rectifying K+ channels, and transcription of genes encoding major inwardly-rectifying K+ channels without affecting ABA-mediated stomatal closure. Overexpression of POTASSIUM CHANNEL IN ARABIDOPSIS THALIANA 1 (KAT1), which encodes a major inwardly-rectifying K+ channel in guard cells, rescued the phenotype of aks1aks2-1 plants. AKS1 bound directly to the promoter of KAT1, an interaction that was attenuated after ABA-induced phosphorylation. The ABA agonist pyrabactin induced phosphorylation of AKSs. Our results demonstrate that the AKS family of bHLH transcription factors facilitates stomatal opening through transcription of genes encoding inwardly-rectifying K+ channels, and that ABA suppresses the activity of inwardly-rectifying K+ channel activity by triggering the phosphorylation of these transcription factors. Microarray data have been deposited in the Gene Expression Omnibus with accession number: GSE46574.
2013-06-28 | PXD000235 | Pride
Project description:Pokhilko2013 - TOC1 signalling in Arabidopsis
circadian clock
In this model, Pokhilko
et al. has incorporated the negative transcriptional
regulations of the core clock genes by TOC1 and the up-regulation
of TOC1 expression by ABA signalling, to their previous model
BIOMD0000000412
This model is described in the article:
Modelling the widespread
effects of TOC1 signalling on the plant circadian clock and its
outputs.
Pokhilko A, Mas P, Millar AJ.
BMC Syst Biol 2013; 7: 23
Abstract:
BACKGROUND: 24-hour biological clocks are intimately
connected to the cellular signalling network, which complicates
the analysis of clock mechanisms. The transcriptional regulator
TOC1 (TIMING OF CAB EXPRESSION 1) is a founding component of
the gene circuit in the plant circadian clock. Recent results
show that TOC1 suppresses transcription of multiple target
genes within the clock circuit, far beyond its
previously-described regulation of the morning transcription
factors LHY (LATE ELONGATED HYPOCOTYL) and CCA1 (CIRCADIAN
CLOCK ASSOCIATED 1). It is unclear how this pervasive effect of
TOC1 affects the dynamics of the clock and its outputs. TOC1
also appears to function in a nested feedback loop that
includes signalling by the plant hormone Abscisic Acid (ABA),
which is upregulated by abiotic stresses, such as drought. ABA
treatments both alter TOC1 levels and affect the clock's timing
behaviour. Conversely, the clock rhythmically modulates
physiological processes induced by ABA, such as the closing of
stomata in the leaf epidermis. In order to understand the
dynamics of the clock and its outputs under changing
environmental conditions, the reciprocal interactions between
the clock and other signalling pathways must be integrated.
RESULTS: We extended the mathematical model of the plant clock
gene circuit by incorporating the repression of multiple clock
genes by TOC1, observed experimentally. The revised model more
accurately matches the data on the clock's molecular profiles
and timing behaviour, explaining the clock's responses in TOC1
over-expression and toc1 mutant plants. A simplified
representation of ABA signalling allowed us to investigate the
interactions of ABA and circadian pathways. Increased ABA
levels lengthen the free-running period of the clock,
consistent with the experimental data. Adding stomatal closure
to the model, as a key ABA- and clock-regulated downstream
process allowed to describe TOC1 effects on the rhythmic gating
of stomatal closure. CONCLUSIONS: The integrated model of the
circadian clock circuit and ABA-regulated environmental sensing
allowed us to explain multiple experimental observations on the
timing and stomatal responses to genetic and environmental
perturbations. These results crystallise a new role of TOC1 as
an environmental sensor, which both affects the pace of the
central oscillator and modulates the kinetics of downstream
processes.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000445.
To cite BioModels Database, please use:
BioModels Database:
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quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
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2013-03-22 | BIOMD0000000445 | BioModels
Project description:Although abscisic acid (ABA) and gibberellins (GAs) play pivotal roles in many physiological processes in plants, their interaction in the control of leaf growth remains elusive. In this study, genetic analyses of ABA and GA interplay in leaf growth were performed in Arabidopsis thaliana. The results indicate that for ABA and GA interaction, leaf growth of both the aba2/ga20ox1 and aba2/GA20OX1-OE plants exhibits partially additive effects but is similar to the aba2 mutant. Consistent with this result, transcriptome analysis suggests that a substantial proportion (45-65%) of the gene expression profile of aba2/ga20ox1 and aba2/GA20OX1-OE plants overlaps and shares a similar pattern to the aba2 mutant. Thus, these data support that ABA deficiency dominates leaf growth regardless of GA levels. Moreover, gene ontology (GO) analysis indicates gene enrichment in the categories of hormone response, developmental and metabolic processes, and cell wall organization in these three genotypes. Leaf developmental genes are also involved in ABA-GA interaction. Collectively, these data support that the genetic relationship of ABA and GA interaction involves multiple coordinated pathways rather than a simple linear pathway in the regulation of leaf growth. To better understand the molecular basis of ABA and GA interaction, transcriptome analysis was performed among the genotypes used in this study.
2015-06-01 | GSE61344 | GEO
Project description:We found that TOR kinase regulates the plant environmental stress responses through phosphorylation at a conserved serine residue of Abscisic acid receptor PYR1/PYLs/RCARs. The phosphorylation inhibits the function of PYLs and prevents the binding of PYLs to abscisic acid and its downstream substrates of PP2C, which blocks the ABA and stress signaling. Our results suggest that plant utilizes this mechanism as a hub to regulate the ABA-mediate stress responses and growth recovery
2017-12-01 | PXD003746 | Pride
Project description:In plants, epidermal guard cells integrate and respond to numerous environmental signals to control stomatal pore apertures thereby regulating gas exchange. Chromatin structure controls transcription factor access to the genome, but whether large-scale chromatin remodeling occurs in guard cells during stomatal movements, and in response to the hormone abscisic acid (ABA) in general, remain unknown. Here we isolate guard cell nuclei from Arabidopsis thaliana plants to examine whether the physiological signals, ABA and CO2, regulate guard cell chromatin during stomatal movements. Our cell type specific analyses uncover patterns of chromatin accessibility specific to guard cells and define novel cis-regulatory sequences supporting guard cell specific gene expression. We find that ABA triggers extensive and dynamic chromatin remodeling in guard cells, roots, and mesophyll cells with clear patterns of cell-type specificity. DNA motif analyses uncover binding sites for distinct transcription factors enriched in ABA-induced and ABA-repressed chromatin. We identify the ABF/AREB bZIP-type transcription factors that are required for ABA-triggered chromatin opening in guard cells and implicate the inhibition of a set of bHLH-type transcription factors in controlling ABA-repressed chromatin. Moreover, we demonstrate that ABA and CO2 induce distinct programs of chromatin remodeling. We provide insight into the control of guard cell chromatin dynamics and propose that ABA-induced chromatin remodeling primes the genome for abiotic stress resistance.
2023-12-19 | GSE243472 | GEO
Project description:In plants, epidermal guard cells integrate and respond to numerous environmental signals to control stomatal pore apertures thereby regulating gas exchange. Chromatin structure controls transcription factor access to the genome, but whether large-scale chromatin remodeling occurs in guard cells during stomatal movements, and in response to the hormone abscisic acid (ABA) in general, remain unknown. Here we isolate guard cell nuclei from Arabidopsis thaliana plants to examine whether the physiological signals, ABA and CO2, regulate guard cell chromatin during stomatal movements. Our cell type specific analyses uncover patterns of chromatin accessibility specific to guard cells and define novel cis-regulatory sequences supporting guard cell specific gene expression. We find that ABA triggers extensive and dynamic chromatin remodeling in guard cells, roots, and mesophyll cells with clear patterns of cell-type specificity. DNA motif analyses uncover binding sites for distinct transcription factors enriched in ABA-induced and ABA-repressed chromatin. We identify the ABF/AREB bZIP-type transcription factors that are required for ABA-triggered chromatin opening in guard cells and implicate the inhibition of a set of bHLH-type transcription factors in controlling ABA-repressed chromatin. Moreover, we demonstrate that ABA and CO2 induce distinct programs of chromatin remodeling. We provide insight into the control of guard cell chromatin dynamics and propose that ABA-induced chromatin remodeling primes the genome for abiotic stress resistance.
2023-12-19 | GSE243470 | GEO
Project description:Abscisic acid (ABA) plays essential roles in plant development and responses to environmental stress. ABA induces subcellular translocation and degradation of the guanine nucleotide exchange factor RopGEF1 thus facilitating ABA core signal transduction. However, the underlying mechanisms for ABA-triggered RopGEF1 trafficking/degradation remain unknown. Studies have revealed that RopGEFs associate with receptor-like kinases to convey developmental signals to small ROP GTPases. However, how the activities of RopGEFs are modulated is not well understood. Type 2C protein phosphatases stabilize the RopGEF1 protein, indicating that phosphorylation may trigger RopGEF1 trafficking and degradation. We have screened inhibitors followed by several protein kinase mutants and find that quadruple mutant plants in the Arabidopsis calcium-dependent protein kinases (CPKs) cpk3/4/6/11 disrupt ABA-induced trafficking and degradation of RopGEF1. Moreover, cpk3/4/6/11 partially impairs ABA inhibition of germination. Several CPKs interact with RopGEF1. CPK4 binds to and phosphorylates RopGEF1 and promotes the degradation of RopGEF1. CPK-mediated phosphorylation of RopGEF1 at specific N-terminal serine residues causes the degradation of RopGEF1 and mutation of these sites also compromises the RopGEF1 over-expression phenotype in root hair development in Arabidopsis. Our findings establish the physiological and molecular functions and relevance of calcium-dependent protein kinases in regulation of RopGEF1 and illuminate physiological roles of a CPK-GEF-ROP module in abscisic acid signaling and plant development. We further discuss that CPK-dependent RopGEF degradation during abiotic stress could provide a mechanism for down-regulation of RopGEF-dependent growth responses.
2019-11-12 | PXD009421 | Pride
Project description:Abscisic acid (ABA) plays essential roles in plant development and responses to environmental stress. ABA induces subcellular translocation and degradation of the guanine nucleotide exchange factor RopGEF1 thus facilitating ABA core signal transduction. However, the underlying mechanisms for ABA-triggered RopGEF1 trafficking/degradation remain unknown. Studies have revealed that RopGEFs associate with receptor-like kinases to convey developmental signals to small ROP GTPases. However, how the activities of RopGEFs are modulated is not well understood. Type 2C protein phosphatases stabilize the RopGEF1 protein, indicating that phosphorylation may trigger RopGEF1 trafficking and degradation. We have screened inhibitors followed by several protein kinase mutants and find that quadruple mutant plants in the Arabidopsis calcium-dependent protein kinases (CPKs) cpk3/4/6/11 disrupt ABA-induced trafficking and degradation of RopGEF1. Moreover, cpk3/4/6/11 partially impairs ABA inhibition of germination. Several CPKs interact with RopGEF1. CPK4 binds to and phosphorylates RopGEF1 and promotes the degradation of RopGEF1. CPK-mediated phosphorylation of RopGEF1 at specific N-terminal serine residues causes the degradation of RopGEF1 and mutation of these sites also compromises the RopGEF1 over-expression phenotype in root hair development in Arabidopsis. Our findings establish the physiological and molecular functions and relevance of calcium-dependent protein kinases in regulation of RopGEF1 and illuminate physiological roles of a CPK-GEF-ROP module in abscisic acid signaling and plant development. We further discuss that CPK-dependent RopGEF degradation during abiotic stress could provide a mechanism for down-regulation of RopGEF-dependent growth responses.
2019-11-12 | PXD009422 | Pride