Serveur d'exploration sur les effecteurs du phytophthora

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A Virulence Essential CRN Effector of Phytophthora capsici Suppresses Host Defense and Induces Cell Death in Plant Nucleus.

Identifieur interne : 000173 ( Main/Exploration ); précédent : 000172; suivant : 000174

A Virulence Essential CRN Effector of Phytophthora capsici Suppresses Host Defense and Induces Cell Death in Plant Nucleus.

Auteurs : Joseph Juma Mafurah [République populaire de Chine] ; Huifei Ma [République populaire de Chine] ; Meixiang Zhang [République populaire de Chine] ; Jing Xu [République populaire de Chine] ; Feng He [République populaire de Chine] ; Tingyue Ye [République populaire de Chine] ; Danyu Shen [République populaire de Chine] ; Yanyu Chen [République populaire de Chine] ; Nasir Ahmed Rajput [République populaire de Chine] ; Daolong Dou [République populaire de Chine]

Source :

RBID : pubmed:26011314

Descripteurs français

English descriptors

Abstract

Phytophthora capsici is a soil-borne plant pathogen with a wide range of hosts. The pathogen secretes a large array of effectors during infection of host plants, including Crinkler (CRN) effectors. However, it remains largely unknown on the roles of these effectors in virulence especially in P. capsici. In this study, we identified a cell death-inducing CRN effector PcCRN4 using agroinfiltration approach. Transient expression of PcCRN4 gene induced cell death in N. benthamiana, N. tabacum and Solanum lycopersicum. Overexpression of the gene in N. benthamiana enhanced susceptibility to P. capsici. Subcellular localization results showed that PcCRN4 localized to the plant nucleus, and the localization was required for both of its cell death-inducing activity and virulent function. Silencing PcCRN4 gene in P. capsici significantly reduced pathogen virulence. The expression of the pathogenesis-related gene PR1b in N. benthamiana was significantly induced when plants were inoculated with PcCRN4-silenced P. capsici transformant compared to the wilt-type. Callose deposits were also abundant at sites inoculated with PcCRN4-silenced transformant, indicating that silencing of PcCRN4 in P. capsici reduced the ability of the pathogen to suppress plant defenses. Transcriptions of cell death-related genes were affected when PcCRN4-silenced line were inoculated on Arabidopsis thaliana, suggesting that PcCRN4 may induce cell death by manipulating cell death-related genes. Overall, our results demonstrate that PcCRN4 is a virulence essential effector and it needs target to the plant nucleus to suppress plant immune responses.

DOI: 10.1371/journal.pone.0127965
PubMed: 26011314
PubMed Central: PMC4444017


Affiliations:


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Le document en format XML

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<keywords scheme="KwdEn" xml:lang="en">
<term>Cell Death (MeSH)</term>
<term>Cell Nucleus (metabolism)</term>
<term>Gene Expression Profiling (MeSH)</term>
<term>Gene Expression Regulation, Plant (MeSH)</term>
<term>Gene Silencing (MeSH)</term>
<term>Genes, Plant (MeSH)</term>
<term>Host-Pathogen Interactions (genetics)</term>
<term>Host-Pathogen Interactions (immunology)</term>
<term>Hydrogen Peroxide (metabolism)</term>
<term>Lycopersicon esculentum (genetics)</term>
<term>Lycopersicon esculentum (immunology)</term>
<term>Lycopersicon esculentum (microbiology)</term>
<term>Nuclear Localization Signals (MeSH)</term>
<term>Phytophthora (pathogenicity)</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>Plants, Genetically Modified (MeSH)</term>
<term>Protein Structure, Tertiary (MeSH)</term>
<term>Proteins (chemistry)</term>
<term>Proteins (metabolism)</term>
<term>Sequence Homology, Amino Acid (MeSH)</term>
<term>Tobacco (genetics)</term>
<term>Tobacco (immunology)</term>
<term>Tobacco (microbiology)</term>
<term>Virulence (MeSH)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr">
<term>Analyse de profil d'expression de gènes (MeSH)</term>
<term>Cellules végétales (microbiologie)</term>
<term>Extinction de l'expression des gènes (MeSH)</term>
<term>Gènes de plante (MeSH)</term>
<term>Immunité des plantes (génétique)</term>
<term>Interactions hôte-pathogène (génétique)</term>
<term>Interactions hôte-pathogène (immunologie)</term>
<term>Lycopersicon esculentum (génétique)</term>
<term>Lycopersicon esculentum (immunologie)</term>
<term>Lycopersicon esculentum (microbiologie)</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>Noyau de la cellule (métabolisme)</term>
<term>Peroxyde d'hydrogène (métabolisme)</term>
<term>Phytophthora (pathogénicité)</term>
<term>Protéines ()</term>
<term>Protéines (métabolisme)</term>
<term>Régulation de l'expression des gènes végétaux (MeSH)</term>
<term>Signaux de localisation nucléaire (MeSH)</term>
<term>Similitude de séquences d'acides aminés (MeSH)</term>
<term>Structure tertiaire des protéines (MeSH)</term>
<term>Tabac (génétique)</term>
<term>Tabac (immunologie)</term>
<term>Tabac (microbiologie)</term>
<term>Virulence (MeSH)</term>
<term>Végétaux génétiquement modifiés (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en">
<term>Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en">
<term>Hydrogen Peroxide</term>
<term>Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en">
<term>Host-Pathogen Interactions</term>
<term>Lycopersicon esculentum</term>
<term>Plant Diseases</term>
<term>Plant Immunity</term>
<term>Tobacco</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr">
<term>Immunité des plantes</term>
<term>Interactions hôte-pathogène</term>
<term>Lycopersicon esculentum</term>
<term>Maladies des plantes</term>
<term>Tabac</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr">
<term>Interactions hôte-pathogène</term>
<term>Lycopersicon esculentum</term>
<term>Maladies des plantes</term>
<term>Tabac</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en">
<term>Host-Pathogen Interactions</term>
<term>Lycopersicon esculentum</term>
<term>Plant Diseases</term>
<term>Tobacco</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en">
<term>Cell Nucleus</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr">
<term>Cellules végétales</term>
<term>Lycopersicon esculentum</term>
<term>Maladies des plantes</term>
<term>Tabac</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiology" xml:lang="en">
<term>Lycopersicon esculentum</term>
<term>Plant Cells</term>
<term>Plant Diseases</term>
<term>Tobacco</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr">
<term>Noyau de la cellule</term>
<term>Peroxyde d'hydrogène</term>
<term>Protéines</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en">
<term>Phytophthora</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr">
<term>Phytophthora</term>
</keywords>
<keywords scheme="MESH" xml:lang="en">
<term>Cell Death</term>
<term>Gene Expression Profiling</term>
<term>Gene Expression Regulation, Plant</term>
<term>Gene Silencing</term>
<term>Genes, Plant</term>
<term>Nuclear Localization Signals</term>
<term>Plants, Genetically Modified</term>
<term>Protein Structure, Tertiary</term>
<term>Sequence Homology, Amino Acid</term>
<term>Virulence</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr">
<term>Analyse de profil d'expression de gènes</term>
<term>Extinction de l'expression des gènes</term>
<term>Gènes de plante</term>
<term>Mort cellulaire</term>
<term>Protéines</term>
<term>Régulation de l'expression des gènes végétaux</term>
<term>Signaux de localisation nucléaire</term>
<term>Similitude de séquences d'acides aminés</term>
<term>Structure tertiaire des protéines</term>
<term>Virulence</term>
<term>Végétaux génétiquement modifiés</term>
</keywords>
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<front>
<div type="abstract" xml:lang="en">Phytophthora capsici is a soil-borne plant pathogen with a wide range of hosts. The pathogen secretes a large array of effectors during infection of host plants, including Crinkler (CRN) effectors. However, it remains largely unknown on the roles of these effectors in virulence especially in P. capsici. In this study, we identified a cell death-inducing CRN effector PcCRN4 using agroinfiltration approach. Transient expression of PcCRN4 gene induced cell death in N. benthamiana, N. tabacum and Solanum lycopersicum. Overexpression of the gene in N. benthamiana enhanced susceptibility to P. capsici. Subcellular localization results showed that PcCRN4 localized to the plant nucleus, and the localization was required for both of its cell death-inducing activity and virulent function. Silencing PcCRN4 gene in P. capsici significantly reduced pathogen virulence. The expression of the pathogenesis-related gene PR1b in N. benthamiana was significantly induced when plants were inoculated with PcCRN4-silenced P. capsici transformant compared to the wilt-type. Callose deposits were also abundant at sites inoculated with PcCRN4-silenced transformant, indicating that silencing of PcCRN4 in P. capsici reduced the ability of the pathogen to suppress plant defenses. Transcriptions of cell death-related genes were affected when PcCRN4-silenced line were inoculated on Arabidopsis thaliana, suggesting that PcCRN4 may induce cell death by manipulating cell death-related genes. Overall, our results demonstrate that PcCRN4 is a virulence essential effector and it needs target to the plant nucleus to suppress plant immune responses. </div>
</front>
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<AbstractText>Phytophthora capsici is a soil-borne plant pathogen with a wide range of hosts. The pathogen secretes a large array of effectors during infection of host plants, including Crinkler (CRN) effectors. However, it remains largely unknown on the roles of these effectors in virulence especially in P. capsici. In this study, we identified a cell death-inducing CRN effector PcCRN4 using agroinfiltration approach. Transient expression of PcCRN4 gene induced cell death in N. benthamiana, N. tabacum and Solanum lycopersicum. Overexpression of the gene in N. benthamiana enhanced susceptibility to P. capsici. Subcellular localization results showed that PcCRN4 localized to the plant nucleus, and the localization was required for both of its cell death-inducing activity and virulent function. Silencing PcCRN4 gene in P. capsici significantly reduced pathogen virulence. The expression of the pathogenesis-related gene PR1b in N. benthamiana was significantly induced when plants were inoculated with PcCRN4-silenced P. capsici transformant compared to the wilt-type. Callose deposits were also abundant at sites inoculated with PcCRN4-silenced transformant, indicating that silencing of PcCRN4 in P. capsici reduced the ability of the pathogen to suppress plant defenses. Transcriptions of cell death-related genes were affected when PcCRN4-silenced line were inoculated on Arabidopsis thaliana, suggesting that PcCRN4 may induce cell death by manipulating cell death-related genes. Overall, our results demonstrate that PcCRN4 is a virulence essential effector and it needs target to the plant nucleus to suppress plant immune responses. </AbstractText>
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