Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Subfamily C7 Raf-like kinases MRK1, RAF26, and RAF39 regulate immune homeostasis and stomatal opening in Arabidopsis thaliana

ABSTRACT: The calcium-dependent protein kinase CPK28 is a regulator of immune homeostasis in multiple plant species. Here, we used a proteomics approach to uncover CPK28-associated proteins. We found that CPK28 associates with subfamily C7 Raf-like kinases MRK1, RAF26, and RAF39, and trans-phosphorylates RAF26 and RAF39. Metazoan Raf kinases function in mitogen-activated protein kinase (MAPK) cascades as MAPK kinase kinases (MKKKs). Although Raf-like kinases share some features with MKKKs, we found that MRK1, RAF26, and RAF39 are unable to trans-phosphorylate any of the 10 Arabidopsis MKKs. We show that MRK1, RAF26, and RAF39 localize to the cytosol and endomembranes, and we define redundant roles for these kinases in stomatal opening, immune-triggered reactive oxygen species (ROS) production, and resistance to a bacterial pathogen. Overall, our study suggests that C7 Raf-like kinases associate with and are phosphorylated by CPK28, function redundantly in stomatal opening and immunity, and possess substrate specificities distinct from canonical MKKKs.

INSTRUMENT(S): Orbitrap Fusion

ORGANISM(S): Arabidopsis Thaliana (mouse-ear Cress)

TISSUE(S): Plant Cell, Plantlet

SUBMITTER: Jan Sklenar

LAB HEAD: Frank Menke

PROVIDER: PXD055293 | Pride | 2024-10-01

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	JM151006R1_A1.MGF	Mgf
	JM151006R1_A1.mzid.gz	Mzid
	JM151006R1_A1.raw	Raw
	JM151006R1_A2.MGF	Mgf
	JM151006R1_A2.mzid.gz	Mzid

Items per page:

1 - 5 of 208

Similar Datasets

Subfamily C7 Raf-like kinases MRK1, RAF26, and RAF39 regulate immune homeostasis and stomatal opening in Arabidopsis thaliana

Project description:The calcium-dependent protein kinase CPK28 is a regulator of immune homeostasis in multiple plant species. Here, we used a proteomics approach to uncover CPK28-associated proteins. We found that CPK28 associates with subfamily C7 Raf-like kinases MRK1, RAF26, and RAF39, and trans-phosphorylates RAF26 and RAF39. Metazoan Raf kinases function in mitogen-activated protein kinase (MAPK) cascades as MAPK kinase kinases (MKKKs). Although Raf-like kinases share some features with MKKKs, we found that MRK1, RAF26, and RAF39 are unable to trans-phosphorylate any of the Arabidopsis MKKs. We show that MRK1, RAF26, and RAF39 localize to the cytosol and endomembranes, and we define redundant roles for these kinases in stomatal opening, immune-triggered reactive oxygen species (ROS) production, and resistance to a bacterial pathogen. Overall, our study suggests that C7 Raf-like kinases associate with and are phosphorylated by CPK28, function redundantly in stomatal immunity, and possess substrate specificities distinct from canonical MKKKs.

2024-09-30 | PXD052803 | Pride

BRAF siRNA NHGRI_Liang_BRAF

Project description:BRAF, one of three RAF serine/threonine kinases (ARAF, BRAF and CRAF), plays a major role in the RAS-RAF-MEK-ERK mitogen-activated protein kinase (MAPK) signaling pathway, which mediates cellular responses to growth signals. Recently a high frequency (~60%-70%) of activating BRAF mutations (predominantly V600E) has been reported in malignant melanoma. In order to identify the downstream effects of BRAF signaling on melanoma cell growth and gene expression, cDNA microarray analysis was carried out following BRAF siRNA or MEK1/2 inhibitor (U0126) treatment. Keywords: time series, siRNA time series, siRNA, drug treatment

2013-07-07 | E-GEOD-5481 | biostudies-arrayexpress

IQGAP1 Scaffold-Kinase Interaction Blockade Selectively Targets Ras-MAP Kinase Driven Tumors

Project description:MAPK scaffolds, such as IQGAP1, assemble pathway kinases together to effect signal transmission and disrupting scaffold function therefore offers a potentially orthogonal approach to MAPK cascade inhibition. Consistent with this possibility, we observed an IQGAP1 requirement in Ras-driven tumorigenesis in mouse and human tissue. Delivery of the IQGAP1 WW peptide sequence that mediates Erk1/4 binding, moreover, disrupted IQGAP1-Erk1/2 interactions, abolished Ras/Raf-driven tumorigenesis, bypassed acquired resistance to the B-Raf inhibitor vemurafinib (PLX- 4032), and acts as a systemically deliverable therapeutic to significantly increase lifespan of tumor bearing mice. Scaffold-kinase interaction blockade (SKIB) acts by a mechanism distinct from direct kinase inhibition and represents a strategy to target over-active oncogenic kinase cascades in cancer. Gene expression profiling: Fragmented cRNA was hybridized to the Mouse Gene 1.0 ST Array (Affymetrix). Iqgap1 wild-type and Iqgap1 knockout mouse treated with topical 4OHT for 0 days and 6 days days are compared.

2013-04-01 | E-GEOD-44967 | biostudies-arrayexpress

IQGAP1 Scaffold-Kinase Interaction Blockade Selectively Targets Ras-MAP Kinase Driven Tumors

2013-04-01 | GSE44967 | GEO

BRAF siRNA NHGRI_Liang_BRAF

2013-07-07 | GSE5481 | GEO

Stomatal opening under high temperatures is controlled by the OST1-regulated TOT3–AHA1 module

Project description:Plants continuously respond to changing environmental conditions to prevent damage and maintain optimal performance. To regulate gas exchange with the environment and to control abiotic stress relief, plants have pores in their leaf epidermis, called stomata. Multiple environmental signals affect the opening and closing of these stomata. High temperatures promote stomatal opening (to cool down), and drought induces stomatal closing (to prevent water loss). Coinciding stress conditions may evoke conflicting stomatal responses, but the cellular mechanisms to resolve these conflicts are unknown. Here we demonstrate that the high-temperature-associated kinase TARGET OF TEMPERATURE 3 directly controls the activity of plasma membrane H+-ATPases to induce stomatal opening. OPEN STOMATA 1, which regulates stomatal closure to prevent water loss during drought stress, directly inactivates TARGET OF TEMPERATURE 3 through phosphorylation. Taken together, this signalling axis harmonizes stomatal opening and closing under high temperatures and drought. In the context of global climate change, understanding how different stress signals converge on stomatal regulation allows the development of climate-change-ready crops.

2024-11-12 | PXD044300 | Pride

Genome-wide Sequencing Facilitates Quantitative Analysis of Wild Type and CRAF-/- cells

Project description:We utilized C-Raf-knockout cell model and carried out RNA-seq analysis of the global transcriptomes in wild-type and C-Raf-knockout cells treated with EGF, a potent activator of MAPK (Mitogen-activated protein kinase) pathway, or vehicle control.

2020-10-27 | GSE106966 | GEO

Durable Suppression of Acquired MEK Inhibitor Resistance in Cancer by Sequestering MEK from ERK and Promoting Anti-Tumor T-cell Immunity [single-cell RNA-seq]

Project description:Disruption of the MAPK pathway in cancer by kinase inhibition often fails due to pathway reactivation, causing clinical relapse. Among MAPK inhibitors, type I RAF inhibitors are only active against specific BRAF mutants; MEK inhibitor monotherapy is associated with limited clinical benefits but may serve as a foundation for combinatorial therapy. Here, we show that type II RAF plus allosteric MEK inhibitors durably blunt the development of acquired MEK inhibitor resistance among cancers with KRAS, NRAS, NF1, BRAFnon-V600 and BRAFV600 mutations, when compared to a combination of type II RAF plus ERK inhibitors. Type II RAF and MEK (versus ERK) inhibitors also display superior capacity to sequester MEK in RAF complexes and uncouple MEK and ERK interaction in acquired resistant tumor subpopulations. Systemically and intratumorally, type II RAF plus MEK inhibitors expand memory and activated/exhausted CD8+ T-cells. Whereas trametinib alone temporally reduces dominant intra-tumoral T-cell clones, type II RAF inhibitor co-treatment reverses this effect and promotes T-cell clonotypic expansion and convergence. Importantly, durably control of tumors by this combination requires CD8+ T-cells. Thus, the prolonged anti-tumor efficacy of type II RAF plus MEK inhibitors reveals exquisite MAPK addiction in common lethal cancer histologies, and the mechanisms include unexpected allosteric perturbation of the MAPK pathway and engagement of anti-tumor CD8+ T-cell immunity.

2021-06-06 | GSE158609 | GEO