A Phytophthora Effector Manipulates Host Histone Acetylation and Reprograms Defense Gene Expression to Promote Infection.
Identifieur interne : 000A12 ( Main/Corpus ); précédent : 000A11; suivant : 000A13A Phytophthora Effector Manipulates Host Histone Acetylation and Reprograms Defense Gene Expression to Promote Infection.
Auteurs : Liang Kong ; Xufang Qiu ; Jiangang Kang ; Yang Wang ; Han Chen ; Jie Huang ; Min Qiu ; Yao Zhao ; Guanghui Kong ; Zhenchuan Ma ; Yan Wang ; Wenwu Ye ; Suomeng Dong ; Wenbo Ma ; Yuanchao WangSource :
- Current biology : CB [ 1879-0445 ] ; 2017.
English descriptors
- KwdEn :
- Acetylation (MeSH), Fungal Proteins (genetics), Fungal Proteins (metabolism), Gene Expression Regulation, Plant (MeSH), Host-Pathogen Interactions (MeSH), Phytophthora (pathogenicity), Phytophthora (physiology), Plant Immunity (MeSH), Soybeans (genetics), Soybeans (immunology), Soybeans (microbiology), Tobacco (genetics), Tobacco (immunology), Tobacco (microbiology), Transcription, Genetic (MeSH), Virulence (MeSH).
- MESH :
- chemical , genetics : Fungal Proteins.
- chemical , metabolism : Fungal Proteins.
- genetics : Soybeans, Tobacco.
- immunology : Soybeans, Tobacco.
- microbiology : Soybeans, Tobacco.
- pathogenicity : Phytophthora.
- physiology : Phytophthora.
- Acetylation, Gene Expression Regulation, Plant, Host-Pathogen Interactions, Plant Immunity, Transcription, Genetic, Virulence.
Abstract
Immune response during pathogen infection requires extensive transcription reprogramming. A fundamental mechanism of transcriptional regulation is histone acetylation. However, how pathogens interfere with this process to promote disease remains largely unknown. Here we demonstrate that the cytoplasmic effector PsAvh23 produced by the soybean pathogen Phytophthora sojae acts as a modulator of histone acetyltransferase (HAT) in plants. PsAvh23 binds to the ADA2 subunit of the HAT complex SAGA and disrupts its assembly by interfering with the association of ADA2 with the catalytic subunit GCN5. As such, PsAvh23 suppresses H3K9 acetylation mediated by the ADA2/GCN5 module and increases plant susceptibility. Expression of PsAvh23 or silencing of GmADA2/GmGCN5 resulted in misregulation of defense-related genes, most likely due to decreased H3K9 acetylation levels at the corresponding loci. This study highlights an effective counter-defense mechanism by which a pathogen effector suppresses the activation of defense genes by interfering with the function of the HAT complex during infection.
DOI: 10.1016/j.cub.2017.02.044
PubMed: 28318979
Links to Exploration step
pubmed:28318979Le document en format XML
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<author><name sortKey="Wang, Yan" sort="Wang, Yan" uniqKey="Wang Y" first="Yan" last="Wang">Yan Wang</name>
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<author><name sortKey="Ma, Wenbo" sort="Ma, Wenbo" uniqKey="Ma W" first="Wenbo" last="Ma">Wenbo Ma</name>
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<author><name sortKey="Wang, Yuanchao" sort="Wang, Yuanchao" uniqKey="Wang Y" first="Yuanchao" last="Wang">Yuanchao Wang</name>
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<term>Fungal Proteins (genetics)</term>
<term>Fungal Proteins (metabolism)</term>
<term>Gene Expression Regulation, Plant (MeSH)</term>
<term>Host-Pathogen Interactions (MeSH)</term>
<term>Phytophthora (pathogenicity)</term>
<term>Phytophthora (physiology)</term>
<term>Plant Immunity (MeSH)</term>
<term>Soybeans (genetics)</term>
<term>Soybeans (immunology)</term>
<term>Soybeans (microbiology)</term>
<term>Tobacco (genetics)</term>
<term>Tobacco (immunology)</term>
<term>Tobacco (microbiology)</term>
<term>Transcription, Genetic (MeSH)</term>
<term>Virulence (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Fungal Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Fungal Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Soybeans</term>
<term>Tobacco</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Soybeans</term>
<term>Tobacco</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Soybeans</term>
<term>Tobacco</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Phytophthora</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Phytophthora</term>
</keywords>
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<term>Gene Expression Regulation, Plant</term>
<term>Host-Pathogen Interactions</term>
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<front><div type="abstract" xml:lang="en">Immune response during pathogen infection requires extensive transcription reprogramming. A fundamental mechanism of transcriptional regulation is histone acetylation. However, how pathogens interfere with this process to promote disease remains largely unknown. Here we demonstrate that the cytoplasmic effector PsAvh23 produced by the soybean pathogen Phytophthora sojae acts as a modulator of histone acetyltransferase (HAT) in plants. PsAvh23 binds to the ADA2 subunit of the HAT complex SAGA and disrupts its assembly by interfering with the association of ADA2 with the catalytic subunit GCN5. As such, PsAvh23 suppresses H3K9 acetylation mediated by the ADA2/GCN5 module and increases plant susceptibility. Expression of PsAvh23 or silencing of GmADA2/GmGCN5 resulted in misregulation of defense-related genes, most likely due to decreased H3K9 acetylation levels at the corresponding loci. This study highlights an effective counter-defense mechanism by which a pathogen effector suppresses the activation of defense genes by interfering with the function of the HAT complex during infection.</div>
</front>
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<DateCompleted><Year>2018</Year>
<Month>07</Month>
<Day>13</Day>
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<DateRevised><Year>2018</Year>
<Month>07</Month>
<Day>13</Day>
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<Issue>7</Issue>
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<Day>03</Day>
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<Title>Current biology : CB</Title>
<ISOAbbreviation>Curr Biol</ISOAbbreviation>
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<ArticleTitle>A Phytophthora Effector Manipulates Host Histone Acetylation and Reprograms Defense Gene Expression to Promote Infection.</ArticleTitle>
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<Abstract><AbstractText>Immune response during pathogen infection requires extensive transcription reprogramming. A fundamental mechanism of transcriptional regulation is histone acetylation. However, how pathogens interfere with this process to promote disease remains largely unknown. Here we demonstrate that the cytoplasmic effector PsAvh23 produced by the soybean pathogen Phytophthora sojae acts as a modulator of histone acetyltransferase (HAT) in plants. PsAvh23 binds to the ADA2 subunit of the HAT complex SAGA and disrupts its assembly by interfering with the association of ADA2 with the catalytic subunit GCN5. As such, PsAvh23 suppresses H3K9 acetylation mediated by the ADA2/GCN5 module and increases plant susceptibility. Expression of PsAvh23 or silencing of GmADA2/GmGCN5 resulted in misregulation of defense-related genes, most likely due to decreased H3K9 acetylation levels at the corresponding loci. This study highlights an effective counter-defense mechanism by which a pathogen effector suppresses the activation of defense genes by interfering with the function of the HAT complex during infection.</AbstractText>
<CopyrightInformation>Copyright © 2017 The Author(s). Published by Elsevier Ltd.. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kong</LastName>
<ForeName>Liang</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Department of Plant Pathology, Nanjing Agricultural University, Nanjing, Jiangsu 210095, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Qiu</LastName>
<ForeName>Xufang</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Department of Plant Pathology, Nanjing Agricultural University, Nanjing, Jiangsu 210095, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kang</LastName>
<ForeName>Jiangang</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Plant Pathology, Nanjing Agricultural University, Nanjing, Jiangsu 210095, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Yang</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Plant Pathology, Nanjing Agricultural University, Nanjing, Jiangsu 210095, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Han</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>Department of Plant Pathology, Nanjing Agricultural University, Nanjing, Jiangsu 210095, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Huang</LastName>
<ForeName>Jie</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Plant Pathology, Nanjing Agricultural University, Nanjing, Jiangsu 210095, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Qiu</LastName>
<ForeName>Min</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Plant Pathology, Nanjing Agricultural University, Nanjing, Jiangsu 210095, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhao</LastName>
<ForeName>Yao</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Plant Pathology, Nanjing Agricultural University, Nanjing, Jiangsu 210095, China; Department of Plant Pathology and Microbiology, University of California, Riverside, Riverside, CA 92521, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kong</LastName>
<ForeName>Guanghui</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>Department of Plant Pathology, Nanjing Agricultural University, Nanjing, Jiangsu 210095, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ma</LastName>
<ForeName>Zhenchuan</ForeName>
<Initials>Z</Initials>
<AffiliationInfo><Affiliation>Department of Plant Pathology, Nanjing Agricultural University, Nanjing, Jiangsu 210095, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Yan</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Plant Pathology, Nanjing Agricultural University, Nanjing, Jiangsu 210095, China; The Key Laboratory of Integrated Management of Crop Diseases and Pests, Ministry of Education, Nanjing, Jiangsu 210095, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ye</LastName>
<ForeName>Wenwu</ForeName>
<Initials>W</Initials>
<AffiliationInfo><Affiliation>Department of Plant Pathology, Nanjing Agricultural University, Nanjing, Jiangsu 210095, China; The Key Laboratory of Integrated Management of Crop Diseases and Pests, Ministry of Education, Nanjing, Jiangsu 210095, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Dong</LastName>
<ForeName>Suomeng</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Plant Pathology, Nanjing Agricultural University, Nanjing, Jiangsu 210095, China; The Key Laboratory of Integrated Management of Crop Diseases and Pests, Ministry of Education, Nanjing, Jiangsu 210095, China. Electronic address: smdong@njau.edu.cn.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ma</LastName>
<ForeName>Wenbo</ForeName>
<Initials>W</Initials>
<AffiliationInfo><Affiliation>Department of Plant Pathology and Microbiology, University of California, Riverside, Riverside, CA 92521, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Yuanchao</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Plant Pathology, Nanjing Agricultural University, Nanjing, Jiangsu 210095, China; The Key Laboratory of Integrated Management of Crop Diseases and Pests, Ministry of Education, Nanjing, Jiangsu 210095, China. Electronic address: wangyc@njau.edu.cn.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
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<ArticleDate DateType="Electronic"><Year>2017</Year>
<Month>03</Month>
<Day>16</Day>
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<MedlineTA>Curr Biol</MedlineTA>
<NlmUniqueID>9107782</NlmUniqueID>
<ISSNLinking>0960-9822</ISSNLinking>
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<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D005656">Fungal Proteins</NameOfSubstance>
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</ChemicalList>
<CitationSubset>IM</CitationSubset>
<CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>Sci Signal. 2017 Apr 25;10(476):</RefSource>
<PMID Version="1">28442629</PMID>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D000107" MajorTopicYN="N">Acetylation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005656" MajorTopicYN="N">Fungal Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018506" MajorTopicYN="Y">Gene Expression Regulation, Plant</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D054884" MajorTopicYN="Y">Host-Pathogen Interactions</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010838" MajorTopicYN="N">Phytophthora</DescriptorName>
<QualifierName UI="Q000472" MajorTopicYN="Y">pathogenicity</QualifierName>
<QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D057865" MajorTopicYN="N">Plant Immunity</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013025" MajorTopicYN="N">Soybeans</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014026" MajorTopicYN="N">Tobacco</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014158" MajorTopicYN="Y">Transcription, Genetic</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014774" MajorTopicYN="N">Virulence</DescriptorName>
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</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">H3K9ac</Keyword>
<Keyword MajorTopicYN="N">Phytophthora</Keyword>
<Keyword MajorTopicYN="N">PsAvh23</Keyword>
<Keyword MajorTopicYN="N">defense gene expression</Keyword>
<Keyword MajorTopicYN="N">histone acetylation</Keyword>
<Keyword MajorTopicYN="N">plant immunity</Keyword>
<Keyword MajorTopicYN="N">virulence</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2017</Year>
<Month>01</Month>
<Day>14</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2017</Year>
<Month>02</Month>
<Day>17</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2017</Year>
<Month>02</Month>
<Day>20</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2017</Year>
<Month>3</Month>
<Day>21</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2018</Year>
<Month>7</Month>
<Day>14</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2017</Year>
<Month>3</Month>
<Day>21</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">28318979</ArticleId>
<ArticleId IdType="pii">S0960-9822(17)30214-2</ArticleId>
<ArticleId IdType="doi">10.1016/j.cub.2017.02.044</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
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