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A Phytophthora sojae effector PsCRN63 forms homo-/hetero-dimers to suppress plant immunity via an inverted association manner.

Identifieur interne : 000D27 ( Main/Exploration ); précédent : 000D26; suivant : 000D28

A Phytophthora sojae effector PsCRN63 forms homo-/hetero-dimers to suppress plant immunity via an inverted association manner.

Auteurs : Qi Li [République populaire de Chine] ; Meixiang Zhang [République populaire de Chine] ; Danyu Shen [République populaire de Chine] ; Tingli Liu [République populaire de Chine] ; Yanyu Chen [République populaire de Chine] ; Jian-Min Zhou [République populaire de Chine] ; Daolong Dou [République populaire de Chine]

Source :

RBID : pubmed:27243217

Descripteurs français

English descriptors

Abstract

Oomycete pathogens produce a large number of effectors to promote infection. Their mode of action are largely unknown. Here we show that a Phytophthora sojae effector, PsCRN63, suppresses flg22-induced expression of FRK1 gene, a molecular marker in pathogen-associated molecular patterns (PAMP)-triggered immunity (PTI). However, PsCRN63 does not suppress upstream signaling events including flg22-induced MAPK activation and BIK1 phosphorylation, indicating that it acts downstream of MAPK cascades. The PsCRN63-transgenic Arabidopsis plants showed increased susceptibility to bacterial pathogen Pseudomonas syringae pathovar tomato (Pst) DC3000 and oomycete pathogen Phytophthora capsici. The callose deposition were suppressed in PsCRN63-transgenic plants compared with the wild-type control plants. Genes involved in PTI were also down-regulated in PsCRN63-transgenic plants. Interestingly, we found that PsCRN63 forms an dimer that is mediated by inter-molecular interactions between N-terminal and C-terminal domains in an inverted association manner. Furthermore, the N-terminal and C-terminal domains required for the dimerization are widely conserved among CRN effectors, suggesting that homo-/hetero-dimerization of Phytophthora CRN effectors is required to exert biological functions. Indeed, the dimerization was required for PTI suppression and cell death-induction activities of PsCRN63.

DOI: 10.1038/srep26951
PubMed: 27243217
PubMed Central: PMC4886637


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<term>Apoptosis Regulatory Proteins (genetics)</term>
<term>Apoptosis Regulatory Proteins (metabolism)</term>
<term>Arabidopsis (genetics)</term>
<term>Arabidopsis (immunology)</term>
<term>Arabidopsis (microbiology)</term>
<term>Arabidopsis Proteins (genetics)</term>
<term>Arabidopsis Proteins (immunology)</term>
<term>Cell Death (MeSH)</term>
<term>Gene Expression Regulation (MeSH)</term>
<term>Host-Pathogen Interactions (MeSH)</term>
<term>Phosphorylation (MeSH)</term>
<term>Phytophthora (genetics)</term>
<term>Phytophthora (growth & development)</term>
<term>Phytophthora (metabolism)</term>
<term>Plant Cells (immunology)</term>
<term>Plant Cells (microbiology)</term>
<term>Plant Diseases (genetics)</term>
<term>Plant Diseases (immunology)</term>
<term>Plant Diseases (microbiology)</term>
<term>Plant Immunity (genetics)</term>
<term>Plant Leaves (genetics)</term>
<term>Plant Leaves (immunology)</term>
<term>Plant Leaves (microbiology)</term>
<term>Plants, Genetically Modified (MeSH)</term>
<term>Protein Kinases (genetics)</term>
<term>Protein Kinases (immunology)</term>
<term>Protein Multimerization (MeSH)</term>
<term>Protein-Serine-Threonine Kinases (genetics)</term>
<term>Protein-Serine-Threonine Kinases (immunology)</term>
<term>Protoplasts (immunology)</term>
<term>Protoplasts (microbiology)</term>
<term>Pseudomonas syringae (genetics)</term>
<term>Pseudomonas syringae (metabolism)</term>
<term>Signal Transduction (MeSH)</term>
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<term>Arabidopsis (génétique)</term>
<term>Arabidopsis (immunologie)</term>
<term>Arabidopsis (microbiologie)</term>
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<term>Cellules végétales (microbiologie)</term>
<term>Feuilles de plante (génétique)</term>
<term>Feuilles de plante (immunologie)</term>
<term>Feuilles de plante (microbiologie)</term>
<term>Immunité des plantes (génétique)</term>
<term>Interactions hôte-pathogène (MeSH)</term>
<term>Maladies des plantes (génétique)</term>
<term>Maladies des plantes (immunologie)</term>
<term>Maladies des plantes (microbiologie)</term>
<term>Mort cellulaire (MeSH)</term>
<term>Multimérisation de protéines (MeSH)</term>
<term>Phosphorylation (MeSH)</term>
<term>Phytophthora (croissance et développement)</term>
<term>Phytophthora (génétique)</term>
<term>Phytophthora (métabolisme)</term>
<term>Protein kinases (génétique)</term>
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<term>Protein-Serine-Threonine Kinases (génétique)</term>
<term>Protein-Serine-Threonine Kinases (immunologie)</term>
<term>Protoplastes (immunologie)</term>
<term>Protoplastes (microbiologie)</term>
<term>Protéines d'Arabidopsis (génétique)</term>
<term>Protéines d'Arabidopsis (immunologie)</term>
<term>Protéines régulatrices de l'apoptose (composition chimique)</term>
<term>Protéines régulatrices de l'apoptose (génétique)</term>
<term>Protéines régulatrices de l'apoptose (métabolisme)</term>
<term>Pseudomonas syringae (génétique)</term>
<term>Pseudomonas syringae (métabolisme)</term>
<term>Régulation de l'expression des gènes (MeSH)</term>
<term>Transduction du signal (MeSH)</term>
<term>Végétaux génétiquement modifiés (MeSH)</term>
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<keywords scheme="MESH" qualifier="composition chimique" xml:lang="fr">
<term>Protéines régulatrices de l'apoptose</term>
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<term>Phytophthora</term>
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<keywords scheme="MESH" qualifier="genetics" xml:lang="en">
<term>Arabidopsis</term>
<term>Phytophthora</term>
<term>Plant Diseases</term>
<term>Plant Immunity</term>
<term>Plant Leaves</term>
<term>Pseudomonas syringae</term>
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<term>Arabidopsis</term>
<term>Feuilles de plante</term>
<term>Immunité des plantes</term>
<term>Maladies des plantes</term>
<term>Phytophthora</term>
<term>Protein kinases</term>
<term>Protein-Serine-Threonine Kinases</term>
<term>Protéines d'Arabidopsis</term>
<term>Protéines régulatrices de l'apoptose</term>
<term>Pseudomonas syringae</term>
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<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr">
<term>Arabidopsis</term>
<term>Cellules végétales</term>
<term>Feuilles de plante</term>
<term>Maladies des plantes</term>
<term>Protein kinases</term>
<term>Protein-Serine-Threonine Kinases</term>
<term>Protoplastes</term>
<term>Protéines d'Arabidopsis</term>
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<keywords scheme="MESH" qualifier="immunology" xml:lang="en">
<term>Arabidopsis</term>
<term>Plant Cells</term>
<term>Plant Diseases</term>
<term>Plant Leaves</term>
<term>Protoplasts</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en">
<term>Phytophthora</term>
<term>Pseudomonas syringae</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr">
<term>Arabidopsis</term>
<term>Cellules végétales</term>
<term>Feuilles de plante</term>
<term>Maladies des plantes</term>
<term>Protoplastes</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiology" xml:lang="en">
<term>Arabidopsis</term>
<term>Plant Cells</term>
<term>Plant Diseases</term>
<term>Plant Leaves</term>
<term>Protoplasts</term>
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<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr">
<term>Phytophthora</term>
<term>Protéines régulatrices de l'apoptose</term>
<term>Pseudomonas syringae</term>
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<term>Gene Expression Regulation</term>
<term>Host-Pathogen Interactions</term>
<term>Phosphorylation</term>
<term>Plants, Genetically Modified</term>
<term>Protein Multimerization</term>
<term>Signal Transduction</term>
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<term>Interactions hôte-pathogène</term>
<term>Mort cellulaire</term>
<term>Multimérisation de protéines</term>
<term>Phosphorylation</term>
<term>Régulation de l'expression des gènes</term>
<term>Transduction du signal</term>
<term>Végétaux génétiquement modifiés</term>
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<front>
<div type="abstract" xml:lang="en">Oomycete pathogens produce a large number of effectors to promote infection. Their mode of action are largely unknown. Here we show that a Phytophthora sojae effector, PsCRN63, suppresses flg22-induced expression of FRK1 gene, a molecular marker in pathogen-associated molecular patterns (PAMP)-triggered immunity (PTI). However, PsCRN63 does not suppress upstream signaling events including flg22-induced MAPK activation and BIK1 phosphorylation, indicating that it acts downstream of MAPK cascades. The PsCRN63-transgenic Arabidopsis plants showed increased susceptibility to bacterial pathogen Pseudomonas syringae pathovar tomato (Pst) DC3000 and oomycete pathogen Phytophthora capsici. The callose deposition were suppressed in PsCRN63-transgenic plants compared with the wild-type control plants. Genes involved in PTI were also down-regulated in PsCRN63-transgenic plants. Interestingly, we found that PsCRN63 forms an dimer that is mediated by inter-molecular interactions between N-terminal and C-terminal domains in an inverted association manner. Furthermore, the N-terminal and C-terminal domains required for the dimerization are widely conserved among CRN effectors, suggesting that homo-/hetero-dimerization of Phytophthora CRN effectors is required to exert biological functions. Indeed, the dimerization was required for PTI suppression and cell death-induction activities of PsCRN63.</div>
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<ArticleTitle>A Phytophthora sojae effector PsCRN63 forms homo-/hetero-dimers to suppress plant immunity via an inverted association manner.</ArticleTitle>
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<AbstractText>Oomycete pathogens produce a large number of effectors to promote infection. Their mode of action are largely unknown. Here we show that a Phytophthora sojae effector, PsCRN63, suppresses flg22-induced expression of FRK1 gene, a molecular marker in pathogen-associated molecular patterns (PAMP)-triggered immunity (PTI). However, PsCRN63 does not suppress upstream signaling events including flg22-induced MAPK activation and BIK1 phosphorylation, indicating that it acts downstream of MAPK cascades. The PsCRN63-transgenic Arabidopsis plants showed increased susceptibility to bacterial pathogen Pseudomonas syringae pathovar tomato (Pst) DC3000 and oomycete pathogen Phytophthora capsici. The callose deposition were suppressed in PsCRN63-transgenic plants compared with the wild-type control plants. Genes involved in PTI were also down-regulated in PsCRN63-transgenic plants. Interestingly, we found that PsCRN63 forms an dimer that is mediated by inter-molecular interactions between N-terminal and C-terminal domains in an inverted association manner. Furthermore, the N-terminal and C-terminal domains required for the dimerization are widely conserved among CRN effectors, suggesting that homo-/hetero-dimerization of Phytophthora CRN effectors is required to exert biological functions. Indeed, the dimerization was required for PTI suppression and cell death-induction activities of PsCRN63.</AbstractText>
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<Affiliation>Department of Plant Pathology, Nanjing Agricultural University, Nanjing 210095, China.</Affiliation>
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<AffiliationInfo>
<Affiliation>Center for Genome Biology and State Key Laboratory of Plant Genomics, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China.</Affiliation>
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<LastName>Zhang</LastName>
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