PhytophthoraV1, Main, Exploration, bibRecord, 000416

Plasmopara viticola effector PvRXLR131 suppresses plant immunity by targeting plant receptor-like kinase inhibitor BKI1.

Identifieur interne : 000416 ( Main/Exploration ); précédent : 000415; suivant : 000417

Plasmopara viticola effector PvRXLR131 suppresses plant immunity by targeting plant receptor-like kinase inhibitor BKI1.

Auteurs : Xia Lan [République populaire de Chine] ; Yunxiao Liu [République populaire de Chine] ; Shiren Song [République populaire de Chine] ; Ling Yin [République populaire de Chine] ; Jiang Xiang [République populaire de Chine] ; Junjie Qu [République populaire de Chine] ; Jiang Lu [République populaire de Chine]

Source :

Molecular plant pathology [ 1364-3703 ] ; 2019.

RBID : pubmed:30945786

Descripteurs français

KwdFr :
- Brassinostéroïdes (métabolisme), Immunité des plantes (génétique), Immunité des plantes (immunologie), Immunité des plantes (physiologie), Maladies des plantes (génétique), Maladies des plantes (microbiologie), Oomycetes (génétique), Oomycetes (immunologie), Oomycetes (pathogénicité), Protéines végétales (génétique), Protéines végétales (métabolisme), Régulation de l'expression des gènes végétaux (génétique), Régulation de l'expression des gènes végétaux (physiologie).
MESH :
- génétique : Immunité des plantes, Maladies des plantes, Oomycetes, Protéines végétales, Régulation de l'expression des gènes végétaux.
- immunologie : Immunité des plantes, Oomycetes.
- microbiologie : Maladies des plantes.
- métabolisme : Brassinostéroïdes, Protéines végétales.
- pathogénicité : Oomycetes.
- physiologie : Immunité des plantes, Régulation de l'expression des gènes végétaux.

English descriptors

KwdEn :
- Brassinosteroids (metabolism), Gene Expression Regulation, Plant (genetics), Gene Expression Regulation, Plant (physiology), Oomycetes (genetics), Oomycetes (immunology), Oomycetes (pathogenicity), Plant Diseases (genetics), Plant Diseases (microbiology), Plant Immunity (genetics), Plant Immunity (immunology), Plant Immunity (physiology), Plant Proteins (genetics), Plant Proteins (metabolism).
MESH :
- chemical , genetics : Plant Proteins.
- chemical , metabolism : Brassinosteroids, Plant Proteins.
- genetics : Gene Expression Regulation, Plant, Oomycetes, Plant Diseases, Plant Immunity.
- immunology : Oomycetes, Plant Immunity.
- microbiology : Plant Diseases.
- pathogenicity : Oomycetes.
- physiology : Gene Expression Regulation, Plant, Plant Immunity.

Abstract

The grapevine downy mildew pathogen Plasmopara viticola secretes a set of RXLR effectors (PvRXLRs) to overcome host immunity and facilitate infection, but how these effectors function is unclear. Here, the biological function of PvRXLR131 was investigated via heterologous expression. Constitutive expression of PvRXLR131 in Colletotrichum gloeosporioides significantly enhanced its pathogenicity on grapevine leaves. Constitutive expression of PvRXLR131 in Arabidopsis promoted Pseudomonas syringae DC3000 and P. syringae DC3000 (hrcC^- ) growth as well as suppressed defence-related callose deposition. Transient expression of PvRXLR131 in Nicotiana benthamiana leaves could also suppress different elicitor-triggered cell death and inhibit plant resistance to Phytophthora capsici. Further analysis revealed that PvRXLR131 interacted with host Vitis vinifera BRI1 kinase inhibitor 1 (VvBKI1), and its homologues in N. benthamiana (NbBKI1) and Arabidopsis (AtBKI1). Moreover, bimolecular fluorescence complementation analysis revealed that PvRXLR131 interacted with VvBKI1 in the plasma membrane. Deletion assays showed that the C-terminus of PvRXLR131 was responsible for the interaction and mutation assays showed that phosphorylation of a conserved tyrosine residue in BKI1s disrupted the interaction. BKI1 was a receptor inhibitor of growth- and defence-related brassinosteroid (BR) and ERECTA (ER) signalling. When silencing of NbBKI1 in N. benthamiana, the virulence function of PvRXLR131 was eliminated, demonstrating that the effector activity is mediated by BKI1. Moreover, PvRXLR131-transgenic plants displayed BKI1-overexpression dwarf phenotypes and suppressed BR and ER signalling. These physiological and genetic data clearly demonstrate that BKI1 is a virulence target of PvRXLR131. We propose that P. viticola secretes PvRXLR131 to target BKI1 as a strategy for promoting infection.

DOI: 10.1111/mpp.12790
PubMed: 30945786
PubMed Central: PMC6637860

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000510
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Le document en format XML

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<term>Gene Expression Regulation, Plant (physiology)</term>
<term>Oomycetes (genetics)</term>
<term>Oomycetes (immunology)</term>
<term>Oomycetes (pathogenicity)</term>
<term>Plant Diseases (genetics)</term>
<term>Plant Diseases (microbiology)</term>
<term>Plant Immunity (genetics)</term>
<term>Plant Immunity (immunology)</term>
<term>Plant Immunity (physiology)</term>
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<term>Plant Proteins (metabolism)</term>
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<term>Immunité des plantes (génétique)</term>
<term>Immunité des plantes (immunologie)</term>
<term>Immunité des plantes (physiologie)</term>
<term>Maladies des plantes (génétique)</term>
<term>Maladies des plantes (microbiologie)</term>
<term>Oomycetes (génétique)</term>
<term>Oomycetes (immunologie)</term>
<term>Oomycetes (pathogénicité)</term>
<term>Protéines végétales (génétique)</term>
<term>Protéines végétales (métabolisme)</term>
<term>Régulation de l'expression des gènes végétaux (génétique)</term>
<term>Régulation de l'expression des gènes végétaux (physiologie)</term>
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<term>Plant Proteins</term>
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<term>Oomycetes</term>
<term>Plant Diseases</term>
<term>Plant Immunity</term>
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<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Immunité des plantes</term>
<term>Maladies des plantes</term>
<term>Oomycetes</term>
<term>Protéines végétales</term>
<term>Régulation de l'expression des gènes végétaux</term>
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<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Immunité des plantes</term>
<term>Oomycetes</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Oomycetes</term>
<term>Plant Immunity</term>
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<front><div type="abstract" xml:lang="en">The grapevine downy mildew pathogen Plasmopara viticola secretes a set of RXLR effectors (PvRXLRs) to overcome host immunity and facilitate infection, but how these effectors function is unclear. Here, the biological function of PvRXLR131 was investigated via heterologous expression. Constitutive expression of PvRXLR131 in Colletotrichum gloeosporioides significantly enhanced its pathogenicity on grapevine leaves. Constitutive expression of PvRXLR131 in Arabidopsis promoted Pseudomonas syringae DC3000 and P. syringae DC3000 (hrcC<sup>-</sup>
 ) growth as well as suppressed defence-related callose deposition. Transient expression of PvRXLR131 in Nicotiana benthamiana leaves could also suppress different elicitor-triggered cell death and inhibit plant resistance to Phytophthora capsici. Further analysis revealed that PvRXLR131 interacted with host Vitis vinifera BRI1 kinase inhibitor 1 (VvBKI1), and its homologues in N. benthamiana (NbBKI1) and Arabidopsis (AtBKI1). Moreover, bimolecular fluorescence complementation analysis revealed that PvRXLR131 interacted with VvBKI1 in the plasma membrane. Deletion assays showed that the C-terminus of PvRXLR131 was responsible for the interaction and mutation assays showed that phosphorylation of a conserved tyrosine residue in BKI1s disrupted the interaction. BKI1 was a receptor inhibitor of growth- and defence-related brassinosteroid (BR) and ERECTA (ER) signalling. When silencing of NbBKI1 in N. benthamiana, the virulence function of PvRXLR131 was eliminated, demonstrating that the effector activity is mediated by BKI1. Moreover, PvRXLR131-transgenic plants displayed BKI1-overexpression dwarf phenotypes and suppressed BR and ER signalling. These physiological and genetic data clearly demonstrate that BKI1 is a virulence target of PvRXLR131. We propose that P. viticola secretes PvRXLR131 to target BKI1 as a strategy for promoting infection.</div>
</front>
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<DateCompleted><Year>2020</Year>
<Month>05</Month>
<Day>04</Day>
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<DateRevised><Year>2020</Year>
<Month>05</Month>
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<JournalIssue CitedMedium="Internet"><Volume>20</Volume>
<Issue>6</Issue>
<PubDate><Year>2019</Year>
<Month>06</Month>
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<Title>Molecular plant pathology</Title>
<ISOAbbreviation>Mol Plant Pathol</ISOAbbreviation>
</Journal>
<ArticleTitle>Plasmopara viticola effector PvRXLR131 suppresses plant immunity by targeting plant receptor-like kinase inhibitor BKI1.</ArticleTitle>
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<Abstract><AbstractText>The grapevine downy mildew pathogen Plasmopara viticola secretes a set of RXLR effectors (PvRXLRs) to overcome host immunity and facilitate infection, but how these effectors function is unclear. Here, the biological function of PvRXLR131 was investigated via heterologous expression. Constitutive expression of PvRXLR131 in Colletotrichum gloeosporioides significantly enhanced its pathogenicity on grapevine leaves. Constitutive expression of PvRXLR131 in Arabidopsis promoted Pseudomonas syringae DC3000 and P. syringae DC3000 (hrcC<sup>-</sup>
 ) growth as well as suppressed defence-related callose deposition. Transient expression of PvRXLR131 in Nicotiana benthamiana leaves could also suppress different elicitor-triggered cell death and inhibit plant resistance to Phytophthora capsici. Further analysis revealed that PvRXLR131 interacted with host Vitis vinifera BRI1 kinase inhibitor 1 (VvBKI1), and its homologues in N. benthamiana (NbBKI1) and Arabidopsis (AtBKI1). Moreover, bimolecular fluorescence complementation analysis revealed that PvRXLR131 interacted with VvBKI1 in the plasma membrane. Deletion assays showed that the C-terminus of PvRXLR131 was responsible for the interaction and mutation assays showed that phosphorylation of a conserved tyrosine residue in BKI1s disrupted the interaction. BKI1 was a receptor inhibitor of growth- and defence-related brassinosteroid (BR) and ERECTA (ER) signalling. When silencing of NbBKI1 in N. benthamiana, the virulence function of PvRXLR131 was eliminated, demonstrating that the effector activity is mediated by BKI1. Moreover, PvRXLR131-transgenic plants displayed BKI1-overexpression dwarf phenotypes and suppressed BR and ER signalling. These physiological and genetic data clearly demonstrate that BKI1 is a virulence target of PvRXLR131. We propose that P. viticola secretes PvRXLR131 to target BKI1 as a strategy for promoting infection.</AbstractText>
<CopyrightInformation>© 2019 The Authors. Molecular Plant Pathology Published by British Society for Plant Pathology and John Wiley & Sons Ltd.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lan</LastName>
<ForeName>Xia</ForeName>
<Initials>X</Initials>
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<AffiliationInfo><Affiliation>College of Food Science and Nutritional Engineering, China Agricultural University, Beijing, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Center for Viticulture and Enology, School of Agriculture and Biology, Shanghai Jiao Tong University, Shanghai, China.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Liu</LastName>
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<AffiliationInfo><Affiliation>Center for Viticulture and Enology, School of Agriculture and Biology, Shanghai Jiao Tong University, Shanghai, China.</Affiliation>
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<Author ValidYN="Y"><LastName>Xiang</LastName>
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Plasmopara viticola effector PvRXLR131 suppresses plant immunity by targeting plant receptor-like kinase inhibitor BKI1.

Plasmopara viticola effector PvRXLR131 suppresses plant immunity by targeting plant receptor-like kinase inhibitor BKI1.

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