Specific Missense Alleles of the Arabidopsis Jasmonic Acid Co-Receptor COI1 Regulate Innate Immune Receptor Accumulation and Function

Autor: David A. Hubert, Eui Hwan Chung, Jeffery L. Dangl, Yijian He, Pablo Tornero
Jazyk: angličtina
Rok vydání: 2012
Předmět:
0106 biological sciences
Pathogen defense
Cancer Research
III effectors
Signaling pathways
Downy mildew resistance
Mutant
Arabidopsis
Cell Cycle Proteins
Plant Science
medicine.disease_cause
01 natural sciences
chemistry.chemical_compound
RNA Processing
Post-Transcriptional
Receptors
Immunologic
Genetics (clinical)
Genetics
0303 health sciences
Mutation
Jasmonic acid
Ubiquitin-Ligase
Intracellular Signaling Peptides and Proteins
Null allele
III Effectors
3. Good health
DNA-Binding Proteins
Jaz proteins
Phenotype
Cop9 signalosome
Signal transduction
Research Article
lcsh:QH426-470
Cyclopentanes
Biology
Nucleotide-Binding site
Signaling Pathways
03 medical and health sciences
medicine
HSP90 Heat-Shock Proteins
Oxylipins
Defense responses
Molecular Biology
Transcription factor
Alleles
Ecology
Evolution
Behavior and Systematics
Plant Diseases
030304 developmental biology
Innate immune system
Arabidopsis Proteins
fungi
Disease resistance protein
Downy Mildew resistance
biology.organism_classification
Immunity
Innate
lcsh:Genetics
chemistry
Nucleotide-binding site
Carrier Proteins
Transcription Factors
010606 plant biology & botany
Zdroj: PLoS Genetics
Digital.CSIC. Repositorio Institucional del CSIC
instname
RiuNet. Repositorio Institucional de la Universitat Politécnica de Valéncia
PLoS Genetics, Vol 8, Iss 10, p e1003018 (2012)
DOI: 10.1371/journal.pgen.1003018
Popis: Plants utilize proteins containing nucleotide binding site (NB) and leucine-rich repeat (LRR) domains as intracellular innate immune receptors to recognize pathogens and initiate defense responses. Since mis-activation of defense responses can lead to tissue damage and even developmental arrest, proper regulation of NB–LRR protein signaling is critical. RAR1, SGT1, and HSP90 act as regulatory chaperones of pre-activation NB–LRR steady-state proteins. We extended our analysis of mutants derived from a rar1 suppressor screen and present two allelic rar1 suppressor (rsp) mutations of Arabidopsis COI1. Like all other coi1 mutations, coi1rsp missense mutations impair Jasmonic Acid (JA) signaling resulting in JA–insensitivity. However, unlike previously identified coi1 alleles, both coi1rsp alleles lack a male sterile phenotype. The coi1rsp mutants express two sets of disease resistance phenotypes. The first, also observed in coi1-1 null allele, includes enhanced basal defense against the virulent bacterial pathogen Pto DC3000 and enhanced effector-triggered immunity (ETI) mediated by the NB–LRR RPM1 protein in both rar1 and wild-type backgrounds. These enhanced disease resistance phenotypes depend on the JA signaling function of COI1. Additionally, the coi1rsp mutants showed a unique inability to properly regulate RPM1 accumulation and HR, exhibited increased RPM1 levels in rar1, and weakened RPM1-mediated HR in RAR1. Importantly, there was no change in the steady-state levels or HR function of RPM1 in coi1-1. These results suggest that the coi1rsp proteins regulate NB–LRR protein accumulation independent of JA signaling. Based on the phenotypic similarities and genetic interactions among coi1rsp, sgt1b, and hsp90.2rsp mutants, our data suggest that COI1 affects NB–LRR accumulation via two NB–LRR co-chaperones, SGT1b and HSP90. Together, our data demonstrate a role for COI1 in disease resistance independent of JA signaling and provide a molecular link between the JA and NB–LRR signaling pathways.
Funding: JLD is a Howard Hughes Medical Institute–Gordon and Betty Moore Foundation Plant Science Investigator. This work was funded by the HHMI–GBMF and by the National Science Foundation (Arabidopsis 2010 Program Grant IOS-0929410 to JLD). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Databáze: OpenAIRE
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