PhytophthoraV1, Main, Exploration, bibRecord, 000695

Plant pathogen effector utilizes host susceptibility factor NRL1 to degrade the immune regulator SWAP70.

Identifieur interne : 000695 ( Main/Exploration ); précédent : 000694; suivant : 000696

Plant pathogen effector utilizes host susceptibility factor NRL1 to degrade the immune regulator SWAP70.

Auteurs : Qin He [Royaume-Uni] ; Shaista Naqvi [Royaume-Uni] ; Hazel Mclellan [Royaume-Uni] ; Petra C. Boevink [Royaume-Uni] ; Nicolas Champouret [États-Unis] ; Ingo Hein [Royaume-Uni] ; Paul R J. Birch [Royaume-Uni]

Source :

Proceedings of the National Academy of Sciences of the United States of America [ 1091-6490 ] ; 2018.

RBID : pubmed:30049706

Descripteurs français

English descriptors

KwdEn :
- Cullin Proteins (genetics), Cullin Proteins (immunology), DNA-Binding Proteins (genetics), DNA-Binding Proteins (immunology), Gene Expression Regulation, Plant (genetics), Gene Expression Regulation, Plant (immunology), Phytophthora infestans (immunology), Plant Diseases (genetics), Plant Diseases (immunology), Plant Immunity (MeSH), Plant Proteins (genetics), Plant Proteins (immunology), Proteolysis (MeSH), Tobacco (genetics), Tobacco (immunology), Tobacco (microbiology).
MESH :
- chemical , genetics : Cullin Proteins, DNA-Binding Proteins, Plant Proteins.
- chemical , immunology : Cullin Proteins, DNA-Binding Proteins, Plant Proteins.
- genetics : Gene Expression Regulation, Plant, Plant Diseases, Tobacco.
- immunology : Gene Expression Regulation, Plant, Phytophthora infestans, Plant Diseases, Tobacco.
- microbiology : Tobacco.
- Plant Immunity, Proteolysis.

Abstract

Plant pathogens deliver effectors into plant cells to suppress immunity. Whereas many effectors inactivate positive immune regulators, other effectors associate with negative regulators of immunity: so-called susceptibility (S) factors. Little is known about how pathogens exploit S factors to suppress immunity. Phytophthora infestans RXLR effector Pi02860 interacts with host protein NRL1, which is an S factor whose activity suppresses INF1-triggered cell death (ICD) and is required for late blight disease. We show that NRL1 interacts in yeast and in planta with a guanine nucleotide exchange factor called SWAP70. SWAP70 associates with endosomes and is a positive regulator of immunity. Virus-induced gene silencing of SWAP70 in Nicotiana benthamiana enhances P. infestans colonization and compromises ICD. In contrast, transient overexpression of SWAP70 reduces P. infestans infection and accelerates ICD. Expression of Pi02860 and NRL1, singly or in combination, results in proteasome-mediated degradation of SWAP70. Degradation of SWAP70 is prevented by silencing NRL1, or by mutation of Pi02860 to abolish its interaction with NRL1. NRL1 is a BTB-domain protein predicted to form the substrate adaptor component of a CULLIN3 ubiquitin E3 ligase. A dimerization-deficient mutant, NRL1^NQ, fails to interact with SWAP70 but maintains its interaction with Pi02860. NRL1^NQ acts as a dominant-negative mutant, preventing SWAP70 degradation in the presence of effector Pi02860, and reducing P. infestans infection. Critically, Pi02860 enhances the association between NRL1 and SWAP70 to promote proteasome-mediated degradation of the latter and, thus, suppress immunity. Preventing degradation of SWAP70 represents a strategy to combat late blight disease.

DOI: 10.1073/pnas.1808585115
PubMed: 30049706
PubMed Central: PMC6099861

Affiliations:

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Le document en format XML

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<term>Cullin Proteins (immunology)</term>
<term>DNA-Binding Proteins (genetics)</term>
<term>DNA-Binding Proteins (immunology)</term>
<term>Gene Expression Regulation, Plant (genetics)</term>
<term>Gene Expression Regulation, Plant (immunology)</term>
<term>Phytophthora infestans (immunology)</term>
<term>Plant Diseases (genetics)</term>
<term>Plant Diseases (immunology)</term>
<term>Plant Immunity (MeSH)</term>
<term>Plant Proteins (genetics)</term>
<term>Plant Proteins (immunology)</term>
<term>Proteolysis (MeSH)</term>
<term>Tobacco (genetics)</term>
<term>Tobacco (immunology)</term>
<term>Tobacco (microbiology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Cullines (génétique)</term>
<term>Cullines (immunologie)</term>
<term>Immunité des plantes (MeSH)</term>
<term>Maladies des plantes (génétique)</term>
<term>Maladies des plantes (immunologie)</term>
<term>Phytophthora infestans (immunologie)</term>
<term>Protéines de liaison à l'ADN (génétique)</term>
<term>Protéines de liaison à l'ADN (immunologie)</term>
<term>Protéines végétales (génétique)</term>
<term>Protéines végétales (immunologie)</term>
<term>Protéolyse (MeSH)</term>
<term>Régulation de l'expression des gènes végétaux (génétique)</term>
<term>Régulation de l'expression des gènes végétaux (immunologie)</term>
<term>Tabac (génétique)</term>
<term>Tabac (immunologie)</term>
<term>Tabac (microbiologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Cullin Proteins</term>
<term>DNA-Binding Proteins</term>
<term>Plant Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Cullin Proteins</term>
<term>DNA-Binding Proteins</term>
<term>Plant Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Gene Expression Regulation, Plant</term>
<term>Plant Diseases</term>
<term>Tobacco</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Cullines</term>
<term>Maladies des plantes</term>
<term>Protéines de liaison à l'ADN</term>
<term>Protéines végétales</term>
<term>Régulation de l'expression des gènes végétaux</term>
<term>Tabac</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Cullines</term>
<term>Maladies des plantes</term>
<term>Phytophthora infestans</term>
<term>Protéines de liaison à l'ADN</term>
<term>Protéines végétales</term>
<term>Régulation de l'expression des gènes végétaux</term>
<term>Tabac</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Gene Expression Regulation, Plant</term>
<term>Phytophthora infestans</term>
<term>Plant Diseases</term>
<term>Tobacco</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Tabac</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Tobacco</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Plant Immunity</term>
<term>Proteolysis</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Immunité des plantes</term>
<term>Protéolyse</term>
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<front><div type="abstract" xml:lang="en">Plant pathogens deliver effectors into plant cells to suppress immunity. Whereas many effectors inactivate positive immune regulators, other effectors associate with negative regulators of immunity: so-called susceptibility (S) factors. Little is known about how pathogens exploit S factors to suppress immunity. <i>Phytophthora infestans</i>
 RXLR effector Pi02860 interacts with host protein NRL1, which is an S factor whose activity suppresses INF1-triggered cell death (ICD) and is required for late blight disease. We show that NRL1 interacts in yeast and <i>in planta</i>
 with a guanine nucleotide exchange factor called SWAP70. SWAP70 associates with endosomes and is a positive regulator of immunity. Virus-induced gene silencing of <i>SWAP70</i>
 in <i>Nicotiana benthamiana</i>
 enhances <i>P. infestans</i>
 colonization and compromises ICD. In contrast, transient overexpression of SWAP70 reduces <i>P. infestans</i>
 infection and accelerates ICD. Expression of Pi02860 and NRL1, singly or in combination, results in proteasome-mediated degradation of SWAP70. Degradation of SWAP70 is prevented by silencing <i>NRL1</i>
, or by mutation of Pi02860 to abolish its interaction with NRL1. NRL1 is a BTB-domain protein predicted to form the substrate adaptor component of a CULLIN3 ubiquitin E3 ligase. A dimerization-deficient mutant, NRL1<sup>NQ</sup>
, fails to interact with SWAP70 but maintains its interaction with Pi02860. NRL1<sup>NQ</sup>
 acts as a dominant-negative mutant, preventing SWAP70 degradation in the presence of effector Pi02860, and reducing <i>P. infestans</i>
 infection. Critically, Pi02860 enhances the association between NRL1 and SWAP70 to promote proteasome-mediated degradation of the latter and, thus, suppress immunity. Preventing degradation of SWAP70 represents a strategy to combat late blight disease.</div>
</front>
</TEI>
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<DateCompleted><Year>2018</Year>
<Month>10</Month>
<Day>02</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>14</Day>
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<Month>08</Month>
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<Title>Proceedings of the National Academy of Sciences of the United States of America</Title>
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<ArticleTitle>Plant pathogen effector utilizes host susceptibility factor NRL1 to degrade the immune regulator SWAP70.</ArticleTitle>
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<Abstract><AbstractText>Plant pathogens deliver effectors into plant cells to suppress immunity. Whereas many effectors inactivate positive immune regulators, other effectors associate with negative regulators of immunity: so-called susceptibility (S) factors. Little is known about how pathogens exploit S factors to suppress immunity. <i>Phytophthora infestans</i>
 RXLR effector Pi02860 interacts with host protein NRL1, which is an S factor whose activity suppresses INF1-triggered cell death (ICD) and is required for late blight disease. We show that NRL1 interacts in yeast and <i>in planta</i>
 with a guanine nucleotide exchange factor called SWAP70. SWAP70 associates with endosomes and is a positive regulator of immunity. Virus-induced gene silencing of <i>SWAP70</i>
 in <i>Nicotiana benthamiana</i>
 enhances <i>P. infestans</i>
 colonization and compromises ICD. In contrast, transient overexpression of SWAP70 reduces <i>P. infestans</i>
 infection and accelerates ICD. Expression of Pi02860 and NRL1, singly or in combination, results in proteasome-mediated degradation of SWAP70. Degradation of SWAP70 is prevented by silencing <i>NRL1</i>
, or by mutation of Pi02860 to abolish its interaction with NRL1. NRL1 is a BTB-domain protein predicted to form the substrate adaptor component of a CULLIN3 ubiquitin E3 ligase. A dimerization-deficient mutant, NRL1<sup>NQ</sup>
, fails to interact with SWAP70 but maintains its interaction with Pi02860. NRL1<sup>NQ</sup>
 acts as a dominant-negative mutant, preventing SWAP70 degradation in the presence of effector Pi02860, and reducing <i>P. infestans</i>
 infection. Critically, Pi02860 enhances the association between NRL1 and SWAP70 to promote proteasome-mediated degradation of the latter and, thus, suppress immunity. Preventing degradation of SWAP70 represents a strategy to combat late blight disease.</AbstractText>
<CopyrightInformation>Copyright © 2018 the Author(s). Published by PNAS.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>He</LastName>
<ForeName>Qin</ForeName>
<Initials>Q</Initials>
<Identifier Source="ORCID">0000-0002-4957-2785</Identifier>
<AffiliationInfo><Affiliation>Division of Plant Science, James Hutton Institute, University of Dundee, Invergowrie, DD2 5DA Dundee, United Kingdom.</Affiliation>
</AffiliationInfo>
</Author>
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</AffiliationInfo>
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</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Hein</LastName>
<ForeName>Ingo</ForeName>
<Initials>I</Initials>
<AffiliationInfo><Affiliation>Division of Plant Science, James Hutton Institute, University of Dundee, Invergowrie, DD2 5DA Dundee, United Kingdom.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Cell and Molecular Sciences, James Hutton Institute, Invergowrie, DD2 5DA Dundee, United Kingdom.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Birch</LastName>
<ForeName>Paul R J</ForeName>
<Initials>PRJ</Initials>
<AffiliationInfo><Affiliation>Division of Plant Science, James Hutton Institute, University of Dundee, Invergowrie, DD2 5DA Dundee, United Kingdom; P.Birch@dundee.ac.uk.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Cell and Molecular Sciences, James Hutton Institute, Invergowrie, DD2 5DA Dundee, United Kingdom.</Affiliation>
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Plant pathogen effector utilizes host susceptibility factor NRL1 to degrade the immune regulator SWAP70.

Plant pathogen effector utilizes host susceptibility factor NRL1 to degrade the immune regulator SWAP70.

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