Overexpression of AtGolS3 and CsRFS in poplar enhances ROS tolerance and represses defense response to leaf rust disease.
Identifieur interne : 000D58 ( Main/Exploration ); précédent : 000D57; suivant : 000D59Overexpression of AtGolS3 and CsRFS in poplar enhances ROS tolerance and represses defense response to leaf rust disease.
Auteurs : Jonathan La Mantia [Canada, États-Unis] ; Faride Unda [Canada] ; Carl J. Douglas [Canada] ; Shawn D. Mansfield [Canada] ; Richard Hamelin [Canada]Source :
- Tree physiology [ 1758-4469 ] ; 2018.
Descripteurs français
- KwdFr :
- Arabidopsis (génétique), Basidiomycota (physiologie), Cucumis sativus (génétique), Espèces réactives de l'oxygène (métabolisme), Maladies des plantes (microbiologie), Populus (génétique), Populus (immunologie), Populus (microbiologie), Régulation de l'expression des gènes végétaux (MeSH), Résistance à la maladie (génétique), Végétaux génétiquement modifiés (génétique), Végétaux génétiquement modifiés (immunologie), Végétaux génétiquement modifiés (microbiologie).
- MESH :
- génétique : Arabidopsis, Cucumis sativus, Populus, Résistance à la maladie, Végétaux génétiquement modifiés.
- immunologie : Populus, Végétaux génétiquement modifiés.
- microbiologie : Maladies des plantes, Populus, Végétaux génétiquement modifiés.
- métabolisme : Espèces réactives de l'oxygène.
- physiologie : Basidiomycota.
- Régulation de l'expression des gènes végétaux.
English descriptors
- KwdEn :
- Arabidopsis (genetics), Basidiomycota (physiology), Cucumis sativus (genetics), Disease Resistance (genetics), Gene Expression Regulation, Plant (MeSH), Plant Diseases (microbiology), Plants, Genetically Modified (genetics), Plants, Genetically Modified (immunology), Plants, Genetically Modified (microbiology), Populus (genetics), Populus (immunology), Populus (microbiology), Reactive Oxygen Species (metabolism).
- MESH :
- chemical , metabolism : Reactive Oxygen Species.
- genetics : Arabidopsis, Cucumis sativus, Disease Resistance, Plants, Genetically Modified, Populus.
- immunology : Plants, Genetically Modified, Populus.
- microbiology : Plant Diseases, Plants, Genetically Modified, Populus.
- physiology : Basidiomycota.
- Gene Expression Regulation, Plant.
Abstract
Plants respond to pathogens through an orchestration of signaling events that coordinate modifications to transcriptional profiles and physiological processes. Resistance to necrotrophic pathogens often requires jasmonic acid, which antagonizes the salicylic acid dependent biotrophic defense response. Recently, myo-inositol has been shown to negatively impact salicylic acid (SA) levels and signaling, while galactinol enhances jasmonic acid (JA)-dependent induced systemic resistance to necrotrophic pathogens. To investigate the function of these compounds in biotrophic pathogen defense, we characterized the defense response of Populus alba × grandidentata overexpressing Arabidopsis GALACTINOL SYNTHASE3 (AtGolS) and Cucumber sativus RAFFINOSE SYNTHASE (CsRFS) challenged with Melampsora aecidiodes, a causative agent of poplar leaf rust disease. Relative to wild-type leaves, the overexpression of AtGolS3 and CsRFS increased accumulation of galactinol and raffinose and led to increased leaf rust infection. During the resistance response, inoculated wild-type leaves displayed reduced levels of galactinol and repressed transcript abundance of two endogenous GolS genes compared to un-inoculated wild-type leaves prior to the up-regulation of NON-EXPRESSOR OF PR1 and PATHOGENESIS-RELATED1. Transcriptome analysis and qRT-PCR validation also revealed the repression of genes participating in calcium influx, phosphatidic acid biosynthesis and signaling, and salicylic acid signaling in the transgenic lines. In contrast, enhanced tolerance to H2O2 and up-regulation of antioxidant biosynthesis genes were exhibited in the overexpression lines. Thus, we conclude that overexpression of AtGolS and CsRFS antagonizes the defense response to poplar leaf rust disease through repressing reactive oxygen species and attenuating calcium and phosphatidic acid signaling events that lead to SA defense.
DOI: 10.1093/treephys/tpx100
PubMed: 28981890
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Mansfield</name><affiliation wicri:level="4"><nlm:affiliation>Department of Wood Science, University of British Columbia, Vancouver BC V6T 1Z4, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Wood Science, University of British Columbia, Vancouver BC V6T 1Z4</wicri:regionArea><orgName type="university">Université de la Colombie-Britannique</orgName><placeName><settlement type="city">Vancouver</settlement><region type="state">Colombie-Britannique </region></placeName></affiliation></author><author><name sortKey="Hamelin, Richard" sort="Hamelin, Richard" uniqKey="Hamelin R" first="Richard" last="Hamelin">Richard Hamelin</name><affiliation wicri:level="4"><nlm:affiliation>Department of Forest and Conservation Sciences, University of British Columbia, Vancouver BC V6T 1Z4, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Forest and Conservation Sciences, University of British Columbia, Vancouver BC V6T 1Z4</wicri:regionArea><orgName type="university">Université de la Colombie-Britannique</orgName><placeName><settlement type="city">Vancouver</settlement><region type="state">Colombie-Britannique </region></placeName></affiliation><affiliation wicri:level="1"><nlm:affiliation>Natural Resources Canada, Laurentian Forestry Center 1055 rue du P.E.P.S., Québec G1V 4C7, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Natural Resources Canada, Laurentian Forestry Center 1055 rue du P.E.P.S., Québec G1V 4C7</wicri:regionArea><wicri:noRegion>Québec G1V 4C7</wicri:noRegion></affiliation></author></analytic><series><title level="j">Tree physiology</title><idno type="eISSN">1758-4469</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Arabidopsis (genetics)</term><term>Basidiomycota (physiology)</term><term>Cucumis sativus (genetics)</term><term>Disease Resistance (genetics)</term><term>Gene Expression Regulation, Plant (MeSH)</term><term>Plant Diseases (microbiology)</term><term>Plants, Genetically Modified (genetics)</term><term>Plants, Genetically Modified (immunology)</term><term>Plants, Genetically Modified (microbiology)</term><term>Populus (genetics)</term><term>Populus (immunology)</term><term>Populus (microbiology)</term><term>Reactive Oxygen Species (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Arabidopsis (génétique)</term><term>Basidiomycota (physiologie)</term><term>Cucumis sativus (génétique)</term><term>Espèces réactives de l'oxygène (métabolisme)</term><term>Maladies des plantes (microbiologie)</term><term>Populus (génétique)</term><term>Populus (immunologie)</term><term>Populus (microbiologie)</term><term>Régulation de l'expression des gènes végétaux (MeSH)</term><term>Résistance à la maladie (génétique)</term><term>Végétaux génétiquement modifiés (génétique)</term><term>Végétaux génétiquement modifiés (immunologie)</term><term>Végétaux génétiquement modifiés (microbiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Reactive Oxygen Species</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Arabidopsis</term><term>Cucumis sativus</term><term>Disease Resistance</term><term>Plants, Genetically Modified</term><term>Populus</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Arabidopsis</term><term>Cucumis sativus</term><term>Populus</term><term>Résistance à la maladie</term><term>Végétaux génétiquement modifiés</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Populus</term><term>Végétaux génétiquement modifiés</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Plants, Genetically Modified</term><term>Populus</term></keywords><keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Maladies des plantes</term><term>Populus</term><term>Végétaux génétiquement modifiés</term></keywords><keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Plant Diseases</term><term>Plants, Genetically Modified</term><term>Populus</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Espèces réactives de l'oxygène</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Basidiomycota</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Basidiomycota</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Gene Expression Regulation, Plant</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Régulation de l'expression des gènes végétaux</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Plants respond to pathogens through an orchestration of signaling events that coordinate modifications to transcriptional profiles and physiological processes. Resistance to necrotrophic pathogens often requires jasmonic acid, which antagonizes the salicylic acid dependent biotrophic defense response. Recently, myo-inositol has been shown to negatively impact salicylic acid (SA) levels and signaling, while galactinol enhances jasmonic acid (JA)-dependent induced systemic resistance to necrotrophic pathogens. To investigate the function of these compounds in biotrophic pathogen defense, we characterized the defense response of Populus alba × grandidentata overexpressing Arabidopsis GALACTINOL SYNTHASE3 (AtGolS) and Cucumber sativus RAFFINOSE SYNTHASE (CsRFS) challenged with Melampsora aecidiodes, a causative agent of poplar leaf rust disease. Relative to wild-type leaves, the overexpression of AtGolS3 and CsRFS increased accumulation of galactinol and raffinose and led to increased leaf rust infection. During the resistance response, inoculated wild-type leaves displayed reduced levels of galactinol and repressed transcript abundance of two endogenous GolS genes compared to un-inoculated wild-type leaves prior to the up-regulation of NON-EXPRESSOR OF PR1 and PATHOGENESIS-RELATED1. Transcriptome analysis and qRT-PCR validation also revealed the repression of genes participating in calcium influx, phosphatidic acid biosynthesis and signaling, and salicylic acid signaling in the transgenic lines. In contrast, enhanced tolerance to H2O2 and up-regulation of antioxidant biosynthesis genes were exhibited in the overexpression lines. Thus, we conclude that overexpression of AtGolS and CsRFS antagonizes the defense response to poplar leaf rust disease through repressing reactive oxygen species and attenuating calcium and phosphatidic acid signaling events that lead to SA defense.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28981890</PMID><DateCompleted><Year>2018</Year><Month>10</Month><Day>24</Day></DateCompleted><DateRevised><Year>2018</Year><Month>10</Month><Day>24</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1758-4469</ISSN><JournalIssue CitedMedium="Internet"><Volume>38</Volume><Issue>3</Issue><PubDate><Year>2018</Year><Month>03</Month><Day>01</Day></PubDate></JournalIssue><Title>Tree physiology</Title><ISOAbbreviation>Tree Physiol</ISOAbbreviation></Journal><ArticleTitle>Overexpression of AtGolS3 and CsRFS in poplar enhances ROS tolerance and represses defense response to leaf rust disease.</ArticleTitle><Pagination><MedlinePgn>457-470</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1093/treephys/tpx100</ELocationID><Abstract><AbstractText>Plants respond to pathogens through an orchestration of signaling events that coordinate modifications to transcriptional profiles and physiological processes. Resistance to necrotrophic pathogens often requires jasmonic acid, which antagonizes the salicylic acid dependent biotrophic defense response. Recently, myo-inositol has been shown to negatively impact salicylic acid (SA) levels and signaling, while galactinol enhances jasmonic acid (JA)-dependent induced systemic resistance to necrotrophic pathogens. To investigate the function of these compounds in biotrophic pathogen defense, we characterized the defense response of Populus alba × grandidentata overexpressing Arabidopsis GALACTINOL SYNTHASE3 (AtGolS) and Cucumber sativus RAFFINOSE SYNTHASE (CsRFS) challenged with Melampsora aecidiodes, a causative agent of poplar leaf rust disease. Relative to wild-type leaves, the overexpression of AtGolS3 and CsRFS increased accumulation of galactinol and raffinose and led to increased leaf rust infection. During the resistance response, inoculated wild-type leaves displayed reduced levels of galactinol and repressed transcript abundance of two endogenous GolS genes compared to un-inoculated wild-type leaves prior to the up-regulation of NON-EXPRESSOR OF PR1 and PATHOGENESIS-RELATED1. Transcriptome analysis and qRT-PCR validation also revealed the repression of genes participating in calcium influx, phosphatidic acid biosynthesis and signaling, and salicylic acid signaling in the transgenic lines. In contrast, enhanced tolerance to H2O2 and up-regulation of antioxidant biosynthesis genes were exhibited in the overexpression lines. Thus, we conclude that overexpression of AtGolS and CsRFS antagonizes the defense response to poplar leaf rust disease through repressing reactive oxygen species and attenuating calcium and phosphatidic acid signaling events that lead to SA defense.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>La Mantia</LastName><ForeName>Jonathan</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Forest and Conservation Sciences, University of British Columbia, Vancouver BC V6T 1Z4, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>United States Department of Agriculture, Wooster, OH 44691, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Unda</LastName><ForeName>Faride</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Department of Wood Science, University of British Columbia, Vancouver BC V6T 1Z4, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Douglas</LastName><ForeName>Carl J</ForeName><Initials>CJ</Initials><AffiliationInfo><Affiliation>Department of Botany, University of British Columbia, Vancouver BC V6T 1Z4, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mansfield</LastName><ForeName>Shawn D</ForeName><Initials>SD</Initials><AffiliationInfo><Affiliation>Department of Wood Science, University of British Columbia, Vancouver BC V6T 1Z4, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hamelin</LastName><ForeName>Richard</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Forest and Conservation Sciences, University of British Columbia, Vancouver BC V6T 1Z4, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Natural Resources Canada, Laurentian Forestry Center 1055 rue du P.E.P.S., Québec G1V 4C7, Canada.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Canada</Country><MedlineTA>Tree Physiol</MedlineTA><NlmUniqueID>100955338</NlmUniqueID><ISSNLinking>0829-318X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017382">Reactive Oxygen Species</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D017360" MajorTopicYN="N">Arabidopsis</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001487" MajorTopicYN="N">Basidiomycota</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018553" MajorTopicYN="N">Cucumis sativus</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D060467" MajorTopicYN="N">Disease Resistance</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018506" MajorTopicYN="Y">Gene Expression Regulation, Plant</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010935" MajorTopicYN="N">Plant Diseases</DescriptorName><QualifierName UI="Q000382" MajorTopicYN="Y">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D030821" MajorTopicYN="N">Plants, Genetically Modified</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="D032107" MajorTopicYN="N">Populus</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2017</Year><Month>03</Month><Day>02</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2017</Year><Month>08</Month><Day>03</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>10</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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sort="Douglas, Carl J" uniqKey="Douglas C" first="Carl J" last="Douglas">Carl J. Douglas</name><name sortKey="Hamelin, Richard" sort="Hamelin, Richard" uniqKey="Hamelin R" first="Richard" last="Hamelin">Richard Hamelin</name><name sortKey="Hamelin, Richard" sort="Hamelin, Richard" uniqKey="Hamelin R" first="Richard" last="Hamelin">Richard Hamelin</name><name sortKey="Mansfield, Shawn D" sort="Mansfield, Shawn D" uniqKey="Mansfield S" first="Shawn D" last="Mansfield">Shawn D. Mansfield</name><name sortKey="Unda, Faride" sort="Unda, Faride" uniqKey="Unda F" first="Faride" last="Unda">Faride Unda</name></country><country name="États-Unis"><region name="Ohio"><name sortKey="La Mantia, Jonathan" sort="La Mantia, Jonathan" uniqKey="La Mantia J" first="Jonathan" last="La Mantia">Jonathan La Mantia</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:28981890" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \
| NlmPubMed2Wicri -a PoplarV1
| This area was generated with Dilib version V0.6.37. |  |