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A Phytophthora Effector Manipulates Host Histone Acetylation and Reprograms Defense Gene Expression to Promote Infection.

Identifieur interne : 000A12 ( Main/Corpus ); précédent : 000A11; suivant : 000A13

A 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 Wang

Source :

RBID : pubmed:28318979

English descriptors

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:28318979

Le document en format XML

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<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>
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<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>
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<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>
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<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>
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<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>
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<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>
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<DescriptorName UI="D014158" MajorTopicYN="Y">Transcription, Genetic</DescriptorName>
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<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>
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<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>
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<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>
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<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>
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