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The tinkerbell (tink) mutation identifies the dual-specificity MAPK phosphatase INDOLE-3-BUTYRIC ACID-RESPONSE5 (IBR5) as a novel regulator of organ size in Arabidopsis.

ABSTRACT: Mitogen-activated dual-specificity MAPK phosphatases are important negative regulators in the MAPK signalling pathways responsible for many essential processes in plants. In a screen for mutants with reduced organ size we have identified a mutation in the active site of the dual-specificity MAPK phosphatase INDOLE-3-BUTYRIC ACID-RESPONSE5 (IBR5) that we named tinkerbell (tink) due to its small size. Analysis of the tink mutant indicates that IBR5 acts as a novel regulator of organ size that changes the rate of growth in petals and leaves. Organ size and shape regulation by IBR5 acts independently of the KLU growth-regulatory pathway. Microarray analysis of tink/ibr5-6 mutants identified a likely role for this phosphatase in male gametophyte development. We show that IBR5 may influence the size and shape of petals through auxin and TCP growth regulatory pathways.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE66419 | GEO | 2015/07/30

SECONDARY ACCESSION(S): PRJNA276853

REPOSITORIES: GEO

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The tinkerbell (tink) mutation identifies the dual-specificity MAPK phosphatase INDOLE-3-BUTYRIC ACID-RESPONSE5 (IBR5) as a novel regulator of organ size in Arabidopsis.

Project description:Mitogen-activated dual-specificity MAPK phosphatases are important negative regulators in the MAPK signalling pathways responsible for many essential processes in plants. In a screen for mutants with reduced organ size we have identified a mutation in the active site of the dual-specificity MAPK phosphatase INDOLE-3-BUTYRIC ACID-RESPONSE5 (IBR5) that we named tinkerbell (tink) due to its small size. Analysis of the tink mutant indicates that IBR5 acts as a novel regulator of organ size that changes the rate of growth in petals and leaves. Organ size and shape regulation by IBR5 acts independently of the KLU growth-regulatory pathway. Microarray analysis of tink/ibr5-6 mutants identified a likely role for this phosphatase in male gametophyte development. We show that IBR5 may influence the size and shape of petals through auxin and TCP growth regulatory pathways. 6 samples, three mutant replicates, three wild type replicates.

2015-07-30 | E-GEOD-66419 | biostudies-arrayexpress

Arabidopsis thaliana

Project description:The tinkerbell (tink) mutation identifies the dual-specificity MAPK phosphatase INDOLE-3-BUTYRIC ACID-RESPONSE5 (IBR5) as a novel regulator of organ size in Arabidopsis.

| PRJNA276853 | ENA

HeLa cell: DUSP2 overexpression vs. control

Project description:The MAPK-specific phosphatase, dual-specificity phosphatase-2 (DUSP2), was negatively regulated by HIF-1a under hypoxia. To identify the downstream genes regulated by DUSP2, microarray analysis was performed. Agilent two color microarray was used to examine the molecular profile after DUSP2 overexpression

2015-09-30 | GSE66656 | GEO

Petals in ranunculaceae - Characterization of the petal gene network in Nigella damascena (Ranunculaceae)

Project description:ngs2013_09_aap-ideev-petals in ranunculaceae-Identification of putative NdAP3-3 target genes-Developmental and genetic origin of shape diversity and evolutionary role.

2021-06-03 | GSE159429 | GEO

Transpositional scaling and niche transitions restore organ size and shape during zebrafish fin regeneration

Project description:Transpositional scaling and niche transitions restore organ size and shape during zebrafish fin regeneration

| PRJNA517717 | ENA

RNA sequencing analysis of WT and Dusp6-/- rat cardiac infiltrated macrophages transcriptomes

Project description:Dual-specificity phosphatase 6 (DUSP6), a member of MAPK phosphatase, serves a specific and conserved function on the dephosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) in multiple species. Utilizing a rat strain harboring nonsense mutation of Dusp6, we found that Dusp6 deficiency improves cardiac function by attenuating cardiomyocyte death and fibrosis in acute inflammatory phase after MI. To investigate the effect of DUSP6 on macrophages in acute inflammatory phase of MI, we performed RNA-seq analysis using CD45+HIS36+ macrophages isolated from Dusp6-deficient and WT infarcted LV tissues 72 h after MI by fluorescent activated cell sorting (FACS).

2022-07-13 | GSE195978 | GEO

The analysis of RhMYB73-interacted proteins in rose by LC-MS

Project description:The size of plant lateral organs is determined by well-coordinated cell proliferation and cell expansion. Here, we report that miR159, an evolutionarily conserved microRNA, plays an essential role in regulating cell division in rose (Rosa hybrida) petals by modulating cytokinin catabolism. We uncovered that Cytokinin Oxidase/Dehydrogenase6 (CKX6) is a target of miR159 in petals. Knocking down miR159 levels resulted in the accumulation of CKX6 transcripts and earlier cytokinin clearance, leading to a shortened cell division period and smaller petals. Conversely, knocking down CKX6 caused cytokinin accumulation and a prolonged developmental cell division period, mimicking the effects of exogenous cytokinin application. MYB73, a R2R3-type MYB transcription repressor, recruited a co-repressor (TOPLESS) and a histone deacetylase (HDA19) to form a suppression complex, which regulated MIR159 expression by modulating histone H3 lysine 9 acetylation levels at the MIR159 promoter. Our work sheds light on mechanisms for ensuring the correct timing of the exit from the cell division phase and thus organ size regulation by controlling cytokinin catabolism.

2023-10-18 | PXD046197 | iProX

Control of LPS-response by DUSP1

Project description:Activation of the Mitogen activated protein kinase (MAPK) cascade following Toll-like receptor (TLR) stimulation enables innate immune cells to rapidly activate cytokine gene expression. A balanced response to signals of infectious danger requires that cellular activation is transient. Here, we identify the MAPK phosphatase Dual specificity phosphatase-1 (DUSP1) as an essential endogenous regulator of the inflammatory response to LPS. DUSP1-deficient (DUSP1-/-) bone marrow derived macrophages showed selectively prolonged activation of p38 MAPK and increased cytokine production. Intraperitoneal challenge of DUSP1-/- mice with LPS caused increased lethality and overshooting production of IL-6 and TNF?. Transcriptional profiling revealed that DUSP1 controls a significant fraction of LPS-induced genes, that includes IL-6 and IL-10 as well as the chemokines CCL3, CCL4 and CXCL2. In contrast, the expression of the important mediators of endotoxin lethality, IFN? and IL-12, was not significantly altered by the absence of DUSP1. These data together demonstrate a specific regulatory role of DUSP1 in controlling a subset of LPS-induced genes that determines the outcome of endotoxin shock. Keywords: in vivo analysis of splenic mRNA expression

2005-12-15 | GSE3565 | GEO

Transcription profiling of spleens from dual specificity phosphatase-1 (DUSP1) deficient and wild type mice to demonstrate a specific regulatory role of DUSP1 on a subset of LPS-induced genes that control the outcome of endotoxin shock.

Project description:Activation of the Mitogen activated protein kinase (MAPK) cascade following Toll-like receptor (TLR) stimulation enables innate immune cells to rapidly activate cytokine gene expression. A balanced response to signals of infectious danger requires that cellular activation is transient. Here, we identify the MAPK phosphatase Dual specificity phosphatase-1 (DUSP1) as an essential endogenous regulator of the inflammatory response to LPS. DUSP1-deficient (DUSP1-/-) bone marrow derived macrophages showed selectively prolonged activation of p38 MAPK and increased cytokine production. Intraperitoneal challenge of DUSP1-/- mice with LPS caused increased lethality and overshooting production of IL-6 and TNF. Transcriptional profiling revealed that DUSP1 controls a significant fraction of LPS-induced genes, that includes IL-6 and IL-10 as well as the chemokines CCL3, CCL4 and CXCL2. In contrast, the expression of the important mediators of endotoxin lethality, IFN? and IL-12, was not significantly altered by the absence of DUSP1. These data together demonstrate a specific regulatory role of DUSP1 in controlling a subset of LPS-induced genes that determines the outcome of endotoxin shock. Experiment Overall Design: Mice were injected intraperitoneally with E. coli LPS (10µg/g bodyweight) and sacrificed 6h later. Total spleen RNA (5 µg) was prepared, labeled and hybridized to Affymetrix MOE430A 2.0 GeneChips according to the manufacturer's instructions. Three biological replicates per condition were analysed. CEL Files were processed for global normalization and generation of expression values using the rma algorithm in the R affy package (www.bioconductor.org).

2007-11-01 | E-GEOD-3565 | biostudies-arrayexpress

Ablation of dual specificity phosphatase 6 protects against non-alcoholic fatty liver disease via CYP4A and MAPK

Project description:Dual specificity phosphatase 6 (DUSP6) is a specific phosphatase for mitogen-activated protein kinase (MAPK). In this study, we used a high-fat diet (HFD)-induced murine non-alcoholic fatty liver disease (NAFLD) model to investigate the role of DUSP6 in this disease. Wild-type (WT) and Dusp6-haploinsufficient (HI) mice developed severe obesity and liver pathology consistent with NAFLD when exposed to HFD. In contrast, Dusp6-knockout (KO) mice completely eliminated these phenotypes. Furthermore, primary hepatocytes isolated from WT mice exposed to palmitic and oleic acids exhibited abundant intracellular lipid accumulation, while hepatocytes from Dusp6-KO mice showed minimal lipid accumulation. Transcriptome analysis revealed significant downregulation of genes encoding cytochrome P450 4A (CYP4A), known to promote ω-hydroxylation of fatty acids and hepatic steatosis, in Dusp6-KO hepatocytes compared with WT hepatocytes. Diminished CYP4A expression was observed in the liver of Dusp6-KO mice compared to WT and Dusp6-HI mice. Knockdown of DUSP6 in HepG2, a human liver-lineage cell line, also promoted a reduction of lipid accumulation, downregulation of CYP4A, and upregulation of phosphorylated/activated MAPK. Furthermore, inhibition of MAPK activity promoted lipid accumulation in DUSP6-knockdown HepG2 cells without affecting CYP4A expression, indicating that CYP4A expression is independent of MAPK activation. These findings highlight the significant role of DUSP6 in HFD-induced steatohepatitis through two distinct pathways involving CYP4A and MAPK.

2023-09-04 | GSE216881 | GEO

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