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An orphan protein of Fusarium graminearum modulates host immunity by mediating proteasomal degradation of TaSnRK1α.

Identifieur interne : 000216 ( Main/Exploration ); précédent : 000215; suivant : 000217

An orphan protein of Fusarium graminearum modulates host immunity by mediating proteasomal degradation of TaSnRK1α.

Auteurs : Cong Jiang [République populaire de Chine, États-Unis] ; Ruonan Hei [République populaire de Chine] ; Yang Yang [République populaire de Chine] ; Shijie Zhang [République populaire de Chine] ; Qinhu Wang [République populaire de Chine] ; Wei Wang [République populaire de Chine] ; Qiang Zhang [République populaire de Chine] ; Min Yan [République populaire de Chine] ; Gengrui Zhu [République populaire de Chine] ; Panpan Huang [République populaire de Chine] ; Huiquan Liu [République populaire de Chine] ; Jin-Rong Xu [États-Unis]

Source :

RBID : pubmed:32873802

Descripteurs français

English descriptors

Abstract

Fusarium graminearum is a causal agent of Fusarium head blight (FHB) and a deoxynivalenol (DON) producer. In this study, OSP24 is identified as an important virulence factor in systematic characterization of the 50 orphan secreted protein (OSP) genes of F. graminearum. Although dispensable for growth and initial penetration, OSP24 is important for infectious growth in wheat rachis tissues. OSP24 is specifically expressed during pathogenesis and its transient expression suppresses BAX- or INF1-induced cell death. Osp24 is translocated into plant cells and two of its 8 cysteine-residues are required for its function. Wheat SNF1-related kinase TaSnRK1α is identified as an Osp24-interacting protein and shows to be important for FHB resistance in TaSnRK1α-overexpressing or silencing transgenic plants. Osp24 accelerates the degradation of TaSnRK1α by facilitating its association with the ubiquitin-26S proteasome. Interestingly, TaSnRK1α also interacts with TaFROG, an orphan wheat protein induced by DON. TaFROG competes against Osp24 for binding with the same region of TaSnRKα and protects it from degradation. Overexpression of TaFROG stabilizes TaSnRK1α and increases FHB resistance. Taken together, Osp24 functions as a cytoplasmic effector by competing against TaFROG for binding with TaSnRK1α, demonstrating the counteracting roles of orphan proteins of both host and fungal pathogens during their interactions.

DOI: 10.1038/s41467-020-18240-y
PubMed: 32873802
PubMed Central: PMC7462860


Affiliations:


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<term>Disease Resistance (MeSH)</term>
<term>Fungal Proteins (metabolism)</term>
<term>Fusarium (immunology)</term>
<term>Fusarium (metabolism)</term>
<term>Fusarium (pathogenicity)</term>
<term>Host-Pathogen Interactions (immunology)</term>
<term>Plant Diseases (immunology)</term>
<term>Plant Diseases (microbiology)</term>
<term>Plant Proteins (genetics)</term>
<term>Plant Proteins (immunology)</term>
<term>Plant Proteins (metabolism)</term>
<term>Plants, Genetically Modified (MeSH)</term>
<term>Proteasome Endopeptidase Complex (metabolism)</term>
<term>Protein-Serine-Threonine Kinases (genetics)</term>
<term>Protein-Serine-Threonine Kinases (immunology)</term>
<term>Protein-Serine-Threonine Kinases (metabolism)</term>
<term>Proteolysis (MeSH)</term>
<term>Trichothecenes (metabolism)</term>
<term>Triticum (immunology)</term>
<term>Triticum (microbiology)</term>
<term>Virulence Factors (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr">
<term>Facteurs de virulence (métabolisme)</term>
<term>Fusarium (immunologie)</term>
<term>Fusarium (métabolisme)</term>
<term>Fusarium (pathogénicité)</term>
<term>Interactions hôte-pathogène (immunologie)</term>
<term>Maladies des plantes (immunologie)</term>
<term>Maladies des plantes (microbiologie)</term>
<term>Proteasome endopeptidase complex (métabolisme)</term>
<term>Protein-Serine-Threonine Kinases (génétique)</term>
<term>Protein-Serine-Threonine Kinases (immunologie)</term>
<term>Protein-Serine-Threonine Kinases (métabolisme)</term>
<term>Protéines fongiques (métabolisme)</term>
<term>Protéines végétales (génétique)</term>
<term>Protéines végétales (immunologie)</term>
<term>Protéines végétales (métabolisme)</term>
<term>Protéolyse (MeSH)</term>
<term>Résistance à la maladie (MeSH)</term>
<term>Trichothécènes (métabolisme)</term>
<term>Triticum (immunologie)</term>
<term>Triticum (microbiologie)</term>
<term>Végétaux génétiquement modifiés (MeSH)</term>
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<term>Plant Proteins</term>
<term>Protein-Serine-Threonine Kinases</term>
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<term>Plant Proteins</term>
<term>Protein-Serine-Threonine Kinases</term>
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<term>Proteasome Endopeptidase Complex</term>
<term>Protein-Serine-Threonine Kinases</term>
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<term>Virulence Factors</term>
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<keywords scheme="MESH" qualifier="génétique" xml:lang="fr">
<term>Protein-Serine-Threonine Kinases</term>
<term>Protéines végétales</term>
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<term>Interactions hôte-pathogène</term>
<term>Maladies des plantes</term>
<term>Protein-Serine-Threonine Kinases</term>
<term>Protéines végétales</term>
<term>Triticum</term>
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<term>Host-Pathogen Interactions</term>
<term>Plant Diseases</term>
<term>Triticum</term>
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<term>Maladies des plantes</term>
<term>Triticum</term>
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<term>Plant Diseases</term>
<term>Triticum</term>
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<term>Facteurs de virulence</term>
<term>Fusarium</term>
<term>Proteasome endopeptidase complex</term>
<term>Protein-Serine-Threonine Kinases</term>
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<term>Protéines végétales</term>
<term>Trichothécènes</term>
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<term>Fusarium</term>
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<term>Fusarium</term>
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<term>Disease Resistance</term>
<term>Plants, Genetically Modified</term>
<term>Proteolysis</term>
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<term>Protéolyse</term>
<term>Résistance à la maladie</term>
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<div type="abstract" xml:lang="en">Fusarium graminearum is a causal agent of Fusarium head blight (FHB) and a deoxynivalenol (DON) producer. In this study, OSP24 is identified as an important virulence factor in systematic characterization of the 50 orphan secreted protein (OSP) genes of F. graminearum. Although dispensable for growth and initial penetration, OSP24 is important for infectious growth in wheat rachis tissues. OSP24 is specifically expressed during pathogenesis and its transient expression suppresses BAX- or INF1-induced cell death. Osp24 is translocated into plant cells and two of its 8 cysteine-residues are required for its function. Wheat SNF1-related kinase TaSnRK1α is identified as an Osp24-interacting protein and shows to be important for FHB resistance in TaSnRK1α-overexpressing or silencing transgenic plants. Osp24 accelerates the degradation of TaSnRK1α by facilitating its association with the ubiquitin-26S proteasome. Interestingly, TaSnRK1α also interacts with TaFROG, an orphan wheat protein induced by DON. TaFROG competes against Osp24 for binding with the same region of TaSnRKα and protects it from degradation. Overexpression of TaFROG stabilizes TaSnRK1α and increases FHB resistance. Taken together, Osp24 functions as a cytoplasmic effector by competing against TaFROG for binding with TaSnRK1α, demonstrating the counteracting roles of orphan proteins of both host and fungal pathogens during their interactions.</div>
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<Title>Nature communications</Title>
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<ArticleTitle>An orphan protein of Fusarium graminearum modulates host immunity by mediating proteasomal degradation of TaSnRK1α.</ArticleTitle>
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<AbstractText>Fusarium graminearum is a causal agent of Fusarium head blight (FHB) and a deoxynivalenol (DON) producer. In this study, OSP24 is identified as an important virulence factor in systematic characterization of the 50 orphan secreted protein (OSP) genes of F. graminearum. Although dispensable for growth and initial penetration, OSP24 is important for infectious growth in wheat rachis tissues. OSP24 is specifically expressed during pathogenesis and its transient expression suppresses BAX- or INF1-induced cell death. Osp24 is translocated into plant cells and two of its 8 cysteine-residues are required for its function. Wheat SNF1-related kinase TaSnRK1α is identified as an Osp24-interacting protein and shows to be important for FHB resistance in TaSnRK1α-overexpressing or silencing transgenic plants. Osp24 accelerates the degradation of TaSnRK1α by facilitating its association with the ubiquitin-26S proteasome. Interestingly, TaSnRK1α also interacts with TaFROG, an orphan wheat protein induced by DON. TaFROG competes against Osp24 for binding with the same region of TaSnRKα and protects it from degradation. Overexpression of TaFROG stabilizes TaSnRK1α and increases FHB resistance. Taken together, Osp24 functions as a cytoplasmic effector by competing against TaFROG for binding with TaSnRK1α, demonstrating the counteracting roles of orphan proteins of both host and fungal pathogens during their interactions.</AbstractText>
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<LastName>Jiang</LastName>
<ForeName>Cong</ForeName>
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<Affiliation>State Key Laboratory of Crop Stress Biology for Arid Areas and NWAFU-Purdue Joint Research Center, College of Plant Protection, Northwest A&F University, 712100, Yangling, Shaanxi, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Department of Botany and Plant Pathology, Purdue University, West Lafayette, IN, 47907, USA.</Affiliation>
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<LastName>Hei</LastName>
<ForeName>Ruonan</ForeName>
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<Affiliation>State Key Laboratory of Crop Stress Biology for Arid Areas and NWAFU-Purdue Joint Research Center, College of Plant Protection, Northwest A&F University, 712100, Yangling, Shaanxi, China.</Affiliation>
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<ForeName>Qinhu</ForeName>
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<Affiliation>State Key Laboratory of Crop Stress Biology for Arid Areas and NWAFU-Purdue Joint Research Center, College of Plant Protection, Northwest A&F University, 712100, Yangling, Shaanxi, China. liuhuiquan@nwsuaf.edu.cn.</Affiliation>
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<AffiliationInfo>
<Affiliation>Department of Botany and Plant Pathology, Purdue University, West Lafayette, IN, 47907, USA. jinrong@purdue.edu.</Affiliation>
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