RNAi silencing of genes for elicitation or biosynthesis of 5-deoxyisoflavonoids suppresses race-specific resistance and hypersensitive cell death in Phytophthora sojae infected tissues.
Identifieur interne : 001E04 ( Main/Exploration ); précédent : 001E03; suivant : 001E05RNAi silencing of genes for elicitation or biosynthesis of 5-deoxyisoflavonoids suppresses race-specific resistance and hypersensitive cell death in Phytophthora sojae infected tissues.
Auteurs : Terrence L. Graham [États-Unis] ; Madge Y. Graham ; Senthil Subramanian ; Oliver YuSource :
- Plant physiology [ 0032-0889 ] ; 2007.
Descripteurs français
- KwdFr :
- Alcohol oxidoreductases (génétique), Alcohol oxidoreductases (métabolisme), Benzopyranes (métabolisme), Espèces réactives de l'oxygène (métabolisme), Interférence par ARN (MeSH), Isoflavones (biosynthèse), Isoflavones (métabolisme), Maladies des plantes (MeSH), Mort cellulaire (physiologie), Oxygénases (génétique), Oxygénases (métabolisme), Phytophthora (physiologie), Protéines végétales (métabolisme), Ptérocarpanes (MeSH), Racines de plante (microbiologie), Racines de plante (métabolisme), Sesquiterpènes (MeSH), Soja (génétique), Soja (microbiologie), Soja (métabolisme), Terpènes (métabolisme).
- MESH :
- biosynthèse : Isoflavones.
- génétique : Alcohol oxidoreductases, Oxygénases, Soja.
- microbiologie : Racines de plante, Soja.
- métabolisme : Alcohol oxidoreductases, Benzopyranes, Espèces réactives de l'oxygène, Isoflavones, Oxygénases, Protéines végétales, Racines de plante, Soja, Terpènes.
- physiologie : Mort cellulaire, Phytophthora.
- Interférence par ARN, Maladies des plantes, Ptérocarpanes, Sesquiterpènes.
English descriptors
- KwdEn :
- Alcohol Oxidoreductases (genetics), Alcohol Oxidoreductases (metabolism), Benzopyrans (metabolism), Cell Death (physiology), Isoflavones (biosynthesis), Isoflavones (metabolism), Oxygenases (genetics), Oxygenases (metabolism), Phytophthora (physiology), Plant Diseases (MeSH), Plant Proteins (metabolism), Plant Roots (metabolism), Plant Roots (microbiology), Pterocarpans (MeSH), RNA Interference (MeSH), Reactive Oxygen Species (metabolism), Sesquiterpenes (MeSH), Soybeans (genetics), Soybeans (metabolism), Soybeans (microbiology), Terpenes (metabolism).
- MESH :
- chemical , biosynthesis : Isoflavones.
- chemical , genetics : Alcohol Oxidoreductases, Oxygenases.
- chemical , metabolism : Alcohol Oxidoreductases, Benzopyrans, Isoflavones, Oxygenases, Plant Proteins, Reactive Oxygen Species, Terpenes.
- genetics : Soybeans.
- metabolism : Plant Roots, Soybeans.
- microbiology : Plant Roots, Soybeans.
- physiology : Cell Death, Phytophthora.
- Plant Diseases, Pterocarpans, RNA Interference, Sesquiterpenes.
Abstract
Isoflavonoids are thought to play an important role in soybean (Glycine max) resistance to Phytophthora sojae. This was addressed by silencing two genes for their biosynthesis and a third gene controlling their elicitation. Silencing of genes for isoflavone synthase (IFS) or chalcone reductase (CHR) was achieved in soybean roots through an Agrobacterium rhizogenes-mediated RNAi approach. Effectiveness of silencing was followed both by quantitative reverse transcriptase-polymerase chain reaction and high-performance liquid chromatography analyses. Silencing either IFS or CHR led to a breakdown of Rps-mediated resistance to race 1 of P. sojae in 'W79' (Rps 1c) or 'W82' (Rps 1k) soybean. Loss of resistance was accompanied by suppression of hypersensitive (HR) cell death in both cultivars and suppression of cell death-associated activation of hydrogen peroxide and peroxidase. The various results suggest that the 5-deoxyisoflavonoids play a critical role in the establishment of cell death and race-specific resistance. The P. sojae cell wall glucan elicitor, a potent elicitor of 5-deoxyisoflavonoids, triggered a cell death response in roots that was also suppressed by silencing either CHR or IFS. Furthermore, silencing of the elicitor-releasing endoglucanase (PR-2) led to a loss of HR cell death and race-specific resistance to P. sojae and also to a loss of isoflavone and cell death responses to cell wall glucan elicitor. Taken together, these results suggest that in situ release of active fragments from a general resistance elicitor (pathogen-associated molecular pattern) is necessary for HR cell death in soybean roots carrying resistance genes at the Rps 1 locus, and that this cell death response is mediated through accumulations of the 5-deoxyisoflavones.
DOI: 10.1104/pp.107.097865
PubMed: 17416637
PubMed Central: PMC1914209
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Graham</name><affiliation wicri:level="1"><nlm:affiliation>Department of Plant Pathology and Plant Molecular Biology and Biotechnology Program, Ohio State University, Columbus, Ohio 43210, USA. graham.1@osu.edu</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Plant Pathology and Plant Molecular Biology and Biotechnology Program, Ohio State University, Columbus, Ohio 43210</wicri:regionArea><wicri:noRegion>Ohio 43210</wicri:noRegion></affiliation></author><author><name sortKey="Graham, Madge Y" sort="Graham, Madge Y" uniqKey="Graham M" first="Madge Y" last="Graham">Madge Y. Graham</name></author><author><name sortKey="Subramanian, Senthil" sort="Subramanian, Senthil" uniqKey="Subramanian S" first="Senthil" last="Subramanian">Senthil Subramanian</name></author><author><name sortKey="Yu, Oliver" sort="Yu, Oliver" uniqKey="Yu O" first="Oliver" last="Yu">Oliver Yu</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2007">2007</date><idno type="RBID">pubmed:17416637</idno><idno type="pmid">17416637</idno><idno type="doi">10.1104/pp.107.097865</idno><idno type="pmc">PMC1914209</idno><idno type="wicri:Area/Main/Corpus">001F82</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">001F82</idno><idno type="wicri:Area/Main/Curation">001F82</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">001F82</idno><idno type="wicri:Area/Main/Exploration">001F82</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">RNAi silencing of genes for elicitation or biosynthesis of 5-deoxyisoflavonoids suppresses race-specific resistance and hypersensitive cell death in Phytophthora sojae infected tissues.</title><author><name sortKey="Graham, Terrence L" sort="Graham, Terrence L" uniqKey="Graham T" first="Terrence L" last="Graham">Terrence L. 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This was addressed by silencing two genes for their biosynthesis and a third gene controlling their elicitation. Silencing of genes for isoflavone synthase (IFS) or chalcone reductase (CHR) was achieved in soybean roots through an Agrobacterium rhizogenes-mediated RNAi approach. Effectiveness of silencing was followed both by quantitative reverse transcriptase-polymerase chain reaction and high-performance liquid chromatography analyses. Silencing either IFS or CHR led to a breakdown of Rps-mediated resistance to race 1 of P. sojae in 'W79' (Rps 1c) or 'W82' (Rps 1k) soybean. Loss of resistance was accompanied by suppression of hypersensitive (HR) cell death in both cultivars and suppression of cell death-associated activation of hydrogen peroxide and peroxidase. The various results suggest that the 5-deoxyisoflavonoids play a critical role in the establishment of cell death and race-specific resistance. The P. sojae cell wall glucan elicitor, a potent elicitor of 5-deoxyisoflavonoids, triggered a cell death response in roots that was also suppressed by silencing either CHR or IFS. Furthermore, silencing of the elicitor-releasing endoglucanase (PR-2) led to a loss of HR cell death and race-specific resistance to P. sojae and also to a loss of isoflavone and cell death responses to cell wall glucan elicitor. Taken together, these results suggest that in situ release of active fragments from a general resistance elicitor (pathogen-associated molecular pattern) is necessary for HR cell death in soybean roots carrying resistance genes at the Rps 1 locus, and that this cell death response is mediated through accumulations of the 5-deoxyisoflavones.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17416637</PMID><DateCompleted><Year>2007</Year><Month>10</Month><Day>02</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0032-0889</ISSN><JournalIssue CitedMedium="Print"><Volume>144</Volume><Issue>2</Issue><PubDate><Year>2007</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Plant physiology</Title><ISOAbbreviation>Plant Physiol</ISOAbbreviation></Journal><ArticleTitle>RNAi silencing of genes for elicitation or biosynthesis of 5-deoxyisoflavonoids suppresses race-specific resistance and hypersensitive cell death in Phytophthora sojae infected tissues.</ArticleTitle><Pagination><MedlinePgn>728-40</MedlinePgn></Pagination><Abstract><AbstractText>Isoflavonoids are thought to play an important role in soybean (Glycine max) resistance to Phytophthora sojae. This was addressed by silencing two genes for their biosynthesis and a third gene controlling their elicitation. Silencing of genes for isoflavone synthase (IFS) or chalcone reductase (CHR) was achieved in soybean roots through an Agrobacterium rhizogenes-mediated RNAi approach. Effectiveness of silencing was followed both by quantitative reverse transcriptase-polymerase chain reaction and high-performance liquid chromatography analyses. Silencing either IFS or CHR led to a breakdown of Rps-mediated resistance to race 1 of P. sojae in 'W79' (Rps 1c) or 'W82' (Rps 1k) soybean. Loss of resistance was accompanied by suppression of hypersensitive (HR) cell death in both cultivars and suppression of cell death-associated activation of hydrogen peroxide and peroxidase. The various results suggest that the 5-deoxyisoflavonoids play a critical role in the establishment of cell death and race-specific resistance. The P. sojae cell wall glucan elicitor, a potent elicitor of 5-deoxyisoflavonoids, triggered a cell death response in roots that was also suppressed by silencing either CHR or IFS. Furthermore, silencing of the elicitor-releasing endoglucanase (PR-2) led to a loss of HR cell death and race-specific resistance to P. sojae and also to a loss of isoflavone and cell death responses to cell wall glucan elicitor. Taken together, these results suggest that in situ release of active fragments from a general resistance elicitor (pathogen-associated molecular pattern) is necessary for HR cell death in soybean roots carrying resistance genes at the Rps 1 locus, and that this cell death response is mediated through accumulations of the 5-deoxyisoflavones.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Graham</LastName><ForeName>Terrence L</ForeName><Initials>TL</Initials><AffiliationInfo><Affiliation>Department of Plant Pathology and Plant Molecular Biology and Biotechnology Program, Ohio State University, Columbus, Ohio 43210, USA. graham.1@osu.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Graham</LastName><ForeName>Madge Y</ForeName><Initials>MY</Initials></Author><Author ValidYN="Y"><LastName>Subramanian</LastName><ForeName>Senthil</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Yu</LastName><ForeName>Oliver</ForeName><Initials>O</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2007</Year><Month>04</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Plant Physiol</MedlineTA><NlmUniqueID>0401224</NlmUniqueID><ISSNLinking>0032-0889</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001578">Benzopyrans</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007529">Isoflavones</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010940">Plant Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D036343">Pterocarpans</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017382">Reactive Oxygen Species</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012717">Sesquiterpenes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D013729">Terpenes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C053376">pathogenesis-related proteins, plant</NameOfSubstance></Chemical><Chemical><RegistryNumber>37297-20-4</RegistryNumber><NameOfSubstance UI="C011991">phytoalexins</NameOfSubstance></Chemical><Chemical><RegistryNumber>6461TV6UCH</RegistryNumber><NameOfSubstance UI="C017343">glyceollin</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.1.-</RegistryNumber><NameOfSubstance UI="D000429">Alcohol Oxidoreductases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.1.1.-</RegistryNumber><NameOfSubstance UI="C093070">chalcone reductase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.13.-</RegistryNumber><NameOfSubstance UI="D010105">Oxygenases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.13.-</RegistryNumber><NameOfSubstance UI="C048489">isoflavone synthase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000429" MajorTopicYN="N">Alcohol Oxidoreductases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001578" MajorTopicYN="N">Benzopyrans</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016923" MajorTopicYN="N">Cell Death</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007529" MajorTopicYN="N">Isoflavones</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="Y">biosynthesis</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010105" MajorTopicYN="N">Oxygenases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010838" MajorTopicYN="N">Phytophthora</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010935" MajorTopicYN="N">Plant Diseases</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010940" MajorTopicYN="N">Plant Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018517" MajorTopicYN="N">Plant Roots</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D036343" MajorTopicYN="N">Pterocarpans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D034622" MajorTopicYN="N">RNA Interference</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012717" MajorTopicYN="N">Sesquiterpenes</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013025" MajorTopicYN="N">Soybeans</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013729" MajorTopicYN="N">Terpenes</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2007</Year><Month>4</Month><Day>10</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>10</Month><Day>3</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2007</Year><Month>4</Month><Day>10</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">17416637</ArticleId><ArticleId IdType="pii">pp.107.097865</ArticleId><ArticleId IdType="doi">10.1104/pp.107.097865</ArticleId><ArticleId 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IdType="pubmed">12232225</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country></list><tree><noCountry><name sortKey="Graham, Madge Y" sort="Graham, Madge Y" uniqKey="Graham M" first="Madge Y" last="Graham">Madge Y. Graham</name><name sortKey="Subramanian, Senthil" sort="Subramanian, Senthil" uniqKey="Subramanian S" first="Senthil" last="Subramanian">Senthil Subramanian</name><name sortKey="Yu, Oliver" sort="Yu, Oliver" uniqKey="Yu O" first="Oliver" last="Yu">Oliver Yu</name></noCountry><country name="États-Unis"><noRegion><name sortKey="Graham, Terrence L" sort="Graham, Terrence L" uniqKey="Graham T" first="Terrence L" last="Graham">Terrence L. Graham</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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