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Expression analysis of Arabidopsis ein2 and bak1 mutants treated with the elicitors elf18 and Pep2.

ABSTRACT: Recognition of microbial patterns and host derived damage signals by host pattern recognition receptors is a key step in immune activation in multicellular eukaryotes. Here we show how mutations in ethylene signaling and the coreceptor bak1 affect host immune responses triggered by elicitors.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE40354 | GEO | 2013/03/05

SECONDARY ACCESSION(S): PRJNA173680

REPOSITORIES: GEO

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Expression analysis of Arabidopsis ein2 and bak1 mutants treated with the elicitors elf18 and Pep2.

Project description:Recognition of microbial patterns and host derived damage signals by host pattern recognition receptors is a key step in immune activation in multicellular eukaryotes. Here we show how mutations in ethylene signaling and the coreceptor bak1 affect host immune responses triggered by elicitors. A 51 DNA microarray study using total RNA from Arabidopsis mutants (ein2-1, bak1-3, efr-1 and pepr1-1 pepr2-3) as well as wild type treated with elf18 or Pep2 with three biological replicates.

2013-03-05 | E-GEOD-40354 | biostudies-arrayexpress

The PXC3 receptor-like kinase constitutively interacts with BAK1 and is involved in vascular development in Arabidopsis.

Project description:We designed an experiment to identify BAK1 interactors considering that it could be a coreceptor for the GOLVEN6 (GLV6) signaling peptide involved in lateral root organogenesis in Arabidopsis thaliana. A BAK1pro:BAK1-GFP/bak1-4 line crossed to an estradiol-inducible GLV6 overexpression line (BAK1pro:BAK1-GFP/bak1-4xiGLV6) was treated with mock or estradiol followed by affinity purification mass spectrometry (AP-MS) experiments using anti-GFP beads in microsomal-enriched fractions. Statistical analysis of estradiol-treated vs. mock seedlings did not reveal significant differences. Nevertheless, we remarked that regardless of the treatment, several LRR-RLKs co-eluted with BAK1-GFP, comprising known, as well as, unknown interactors. We confirmed interaction of BAK1 with these LRR-RLKs by BIFC and identified the PXC3 receptor as a BAK1 constitutive interactor, which was further verified by co-IP.

2022-02-17 | PXD026487 | Pride

Control of lateral root formation by rapamycin-induced dimerization of engineered RGI/BAK1 and by BIR3 chimera

Project description:Leucine-rich repeat receptor kinases (LRR-RKs) play a pivotal role in diverse aspects of growth, development, and immunity in plants by sensing extracellular signals. Typically, LRR-RKs are activated through the ligand-induced interaction with a SOMATIC EMBRYOGENESIS RECEPTOR KINASE (SERK) coreceptor, triggering downstream signaling. ROOT MERISTEM GROWTH FACTOR1 (RGF1) INSENSITIVEs (RGIs) LRR-RLK receptors promote primary root meristem activity while inhibiting lateral root (LR) development in response to RGF peptide. In this study, we employed rapamycin-induced dimerization (RiD) and BAK1-INTERACTING RECEPTOR-LIKE KINASE3 (BIR3) chimera approaches to explore the gain-of-function of RGI1, RGI4, and RGI5. Rapamycin induced the association of cytosolic kinase domains (CKDs) of RGI1 and the BAK1 coreceptor, activating both mitogen-activated protein kinase 3 (MPK3) and MPK6. Rapamycin significantly inhibited LR formation in RiD-RGI1/RGI4/RGI5-BAK1 plants. Using transgenic Arabidopsis expressing RGI1CKD fused to the BIR3-LRR chimera under estradiol control, we observed a substantial reduction in LR density upon β-estradiol treatment. Additionally, we identified a decrease in root gravitropism in BIR3 chimera plants. In contrast, RiD-RGI/BAK1 plants did not exhibit defects in root gravitropism, implying the importance of combinatorial interactions between RGIs and SERK coreceptors in the inhibition of root gravitropism. Constitutive activation of RGIs with BAK1 in RiD-RGI/BAK1 plants by rapamycin treatment resulted in the inhibition of primary root growth, resembling the inhibitory effects observed with high concentrations of phytohormones on primary root elongation. Our findings highlight that the interactions between CKDs of RGIs and BAK1, constitutively induced by rapamycin or BIR3 chimera, efficiently control LR development.

2023-12-21 | GSE138627 | GEO

Deletion of Bak1 alleviates microglial necroptosis and neuroinflammation after experimental subarachnoid hemorrhage

Project description:Microglial necroptosis exacerbates neurodegenerative diseases, central nervous system injury and demonstrates a pro-inflammatory process, but its contribution to subarachnoid hemorrhage (SAH) is poorly characterized. BCL-2 homologous antagonist-killer protein (Bak1), a critical regulatory molecule of endogenous apoptosis, can be involved in the pathological process of necroptosis by regulating mitochondrial permeability. In this study, we revealed microglia undergo necroptosis after subarachnoid hemorrhage in vivo and vitro. We found that Bak1 was elevated at 24h after SAH. Knocked-down of Bak1 by adeno-associated virus attenuates microglial necroptosis, alleviates neuroinflammation, and improves neurological function after SAH. To further explore the corresponding mechanisms, oxyhemoglobin induces necroptosis in BV2 microglia, increasing Bak1 expression and mediating pro-inflammatory phenotype transformation, exacerbating oxidative stress and neuroinflammation. Abrogating BV2 Bak1 reduces necroptosis by downregulating the expression of phosphorylated pseudokinase mixed lineage kinase domain-like protein (p-MLKL), then downregulates pro-inflammatory phenotype gene expression. RNA-Seq shows that disrupting BV2 Bak1 downregulates multiple immune and inflammatory pathways and ameliorates cell injury by elevating Thrombospondin 1 (THBS1) expression. In summary, we identified a critical regulatory role for Bak1 in microglial necroptosis and neuroinflammation after SAH. Bak1 is expected to be a new therapeutic target, and it provides a new idea for the treatment strategy of SAH.

2022-04-10 | GSE200224 | GEO

bak1 bkk1 flg22 - Flagellin response in mpk mutants

Project description:au-09-01_mpk_flagellin_edu - bak1 bkk1 flg22 - Investigate flagellin mpk dependent genes. - 2 weeks Bak1bkk1 plants treated with flg22 1h 1 microM

2012-01-01 | GSE23184 | GEO

bak1 bkk1 flg22 - Flagellin response in mpk mutants

Project description:au-09-01_mpk_flagellin_edu - bak1 bkk1 flg22 - Investigate flagellin mpk dependent genes. - 2 weeks Bak1bkk1 plants treated with flg22 1h 1 microM 2 dye-swap - CATMA arrays

2012-01-01 | E-GEOD-23184 | biostudies-arrayexpress

Genome-wide expression analysis of bri1-5 and its suppressors brs1-1D, bak1-1D, bri1-1D

Project description:bri1-5 is a weak mutant of Brassinosteroid Insensitive 1 (BRI1). Suppressors by activation tagging bri1-1D, brs1-1D and bak1-1D can recover bri1-5 phenotype. We use microarray to investigate which pathways or functional categories have been transcriptionally regulated by bri1-1D, brs1-1D and bak1-1D. Whole seedlings from wild-type (WS2), bri1-5, bri1-5/brs1-1D, bri1-5/bak1-1D, bri1-5/bri1-1D. Three biological replicates for each genotype.

2015-07-14 | E-GEOD-70843 | biostudies-arrayexpress

Genome-wide expression analysis of bri1-5 and its suppressors brs1-1D, bak1-1D, bri1-1D

2015-07-14 | GSE70843 | GEO

Small RNA profiling of Arabidopsis in response to fungal elicitors

Project description:This experiment describes small RNA gene expression after treatment of Arabidopsis seedlings with elicitors obtained from the fungus F. oxysporum

2014-12-01 | GSE59978 | GEO

Transcriptome profiling of Brassica rapa subsp. pekinensis treated with immunity elicitors

Project description:Plant leaf discs were treated with plant immunity elicitors (chitin or flg22) or water for 30 or 180 minutes

2020-05-19 | GSE150746 | GEO