A Phytophthora sojae effector PsCRN63 forms homo-/hetero-dimers to suppress plant immunity via an inverted association manner.
Identifieur interne : 000B92 ( Main/Curation ); précédent : 000B91; suivant : 000B93A 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 :
- Scientific reports [ 2045-2322 ] ; 2016.
Descripteurs français
- KwdFr :
- Arabidopsis (génétique), Arabidopsis (immunologie), Arabidopsis (microbiologie), Cellules végétales (immunologie), Cellules végétales (microbiologie), Feuilles de plante (génétique), Feuilles de plante (immunologie), Feuilles de plante (microbiologie), Immunité des plantes (génétique), Interactions hôte-pathogène (MeSH), Maladies des plantes (génétique), Maladies des plantes (immunologie), Maladies des plantes (microbiologie), Mort cellulaire (MeSH), Multimérisation de protéines (MeSH), Phosphorylation (MeSH), Phytophthora (croissance et développement), Phytophthora (génétique), Phytophthora (métabolisme), Protein kinases (génétique), Protein kinases (immunologie), Protein-Serine-Threonine Kinases (génétique), Protein-Serine-Threonine Kinases (immunologie), Protoplastes (immunologie), Protoplastes (microbiologie), Protéines d'Arabidopsis (génétique), Protéines d'Arabidopsis (immunologie), Protéines régulatrices de l'apoptose (composition chimique), Protéines régulatrices de l'apoptose (génétique), Protéines régulatrices de l'apoptose (métabolisme), Pseudomonas syringae (génétique), Pseudomonas syringae (métabolisme), Régulation de l'expression des gènes (MeSH), Transduction du signal (MeSH), Végétaux génétiquement modifiés (MeSH).
- MESH :
- composition chimique : Protéines régulatrices de l'apoptose.
- croissance et développement : Phytophthora.
- génétique : Arabidopsis, Feuilles de plante, Immunité des plantes, Maladies des plantes, Phytophthora, Protein kinases, Protein-Serine-Threonine Kinases, Protéines d'Arabidopsis, Protéines régulatrices de l'apoptose, Pseudomonas syringae.
- immunologie : Arabidopsis, Cellules végétales, Feuilles de plante, Maladies des plantes, Protein kinases, Protein-Serine-Threonine Kinases, Protoplastes, Protéines d'Arabidopsis.
- microbiologie : Arabidopsis, Cellules végétales, Feuilles de plante, Maladies des plantes, Protoplastes.
- métabolisme : Phytophthora, Protéines régulatrices de l'apoptose, Pseudomonas syringae.
- Interactions hôte-pathogène, Mort cellulaire, Multimérisation de protéines, Phosphorylation, Régulation de l'expression des gènes, Transduction du signal, Végétaux génétiquement modifiés.
English descriptors
- KwdEn :
- Apoptosis Regulatory Proteins (chemistry), Apoptosis Regulatory Proteins (genetics), Apoptosis Regulatory Proteins (metabolism), Arabidopsis (genetics), Arabidopsis (immunology), Arabidopsis (microbiology), Arabidopsis Proteins (genetics), Arabidopsis Proteins (immunology), Cell Death (MeSH), Gene Expression Regulation (MeSH), Host-Pathogen Interactions (MeSH), Phosphorylation (MeSH), Phytophthora (genetics), Phytophthora (growth & development), Phytophthora (metabolism), Plant Cells (immunology), Plant Cells (microbiology), Plant Diseases (genetics), Plant Diseases (immunology), Plant Diseases (microbiology), Plant Immunity (genetics), Plant Leaves (genetics), Plant Leaves (immunology), Plant Leaves (microbiology), Plants, Genetically Modified (MeSH), Protein Kinases (genetics), Protein Kinases (immunology), Protein Multimerization (MeSH), Protein-Serine-Threonine Kinases (genetics), Protein-Serine-Threonine Kinases (immunology), Protoplasts (immunology), Protoplasts (microbiology), Pseudomonas syringae (genetics), Pseudomonas syringae (metabolism), Signal Transduction (MeSH).
- MESH :
- chemical , chemistry : Apoptosis Regulatory Proteins.
- chemical , genetics : Apoptosis Regulatory Proteins, Arabidopsis Proteins, Protein Kinases, Protein-Serine-Threonine Kinases.
- chemical , immunology : Arabidopsis Proteins, Protein Kinases, Protein-Serine-Threonine Kinases.
- chemical , metabolism : Apoptosis Regulatory Proteins.
- genetics : Arabidopsis, Phytophthora, Plant Diseases, Plant Immunity, Plant Leaves, Pseudomonas syringae.
- growth & development : Phytophthora.
- immunology : Arabidopsis, Plant Cells, Plant Diseases, Plant Leaves, Protoplasts.
- metabolism : Phytophthora, Pseudomonas syringae.
- microbiology : Arabidopsis, Plant Cells, Plant Diseases, Plant Leaves, Protoplasts.
- Cell Death, Gene Expression Regulation, Host-Pathogen Interactions, Phosphorylation, Plants, Genetically Modified, Protein Multimerization, Signal Transduction.
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 (immunologie)</term>
<term>Arabidopsis (microbiologie)</term>
<term>Cellules végétales (immunologie)</term>
<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>
<term>Protein kinases (immunologie)</term>
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<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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<term>Protéines d'Arabidopsis</term>
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<term>Plant Cells</term>
<term>Plant Diseases</term>
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<term>Protéines régulatrices de l'apoptose</term>
<term>Pseudomonas syringae</term>
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<term>Host-Pathogen Interactions</term>
<term>Phosphorylation</term>
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<term>Protein Multimerization</term>
<term>Signal Transduction</term>
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<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>
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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>
</front>
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<Abstract><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>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Qi</ForeName>
<Initials>Q</Initials>
<AffiliationInfo><Affiliation>Department of Plant Pathology, Nanjing Agricultural University, Nanjing 210095, China.</Affiliation>
</AffiliationInfo>
<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>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Meixiang</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Plant Pathology, Nanjing Agricultural University, Nanjing 210095, China.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Shen</LastName>
<ForeName>Danyu</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Department of Plant Pathology, Nanjing Agricultural University, Nanjing 210095, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Liu</LastName>
<ForeName>Tingli</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Department of Plant Pathology, Nanjing Agricultural University, Nanjing 210095, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Yanyu</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Plant Pathology, Nanjing Agricultural University, Nanjing 210095, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhou</LastName>
<ForeName>Jian-Min</ForeName>
<Initials>JM</Initials>
<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>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Dou</LastName>
<ForeName>Daolong</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Department of Plant Pathology, Nanjing Agricultural University, Nanjing 210095, China.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
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<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
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<ArticleDate DateType="Electronic"><Year>2016</Year>
<Month>05</Month>
<Day>31</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>England</Country>
<MedlineTA>Sci Rep</MedlineTA>
<NlmUniqueID>101563288</NlmUniqueID>
<ISSNLinking>2045-2322</ISSNLinking>
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