Nicotiflorin, rutin and chlorogenic acid: phenylpropanoids involved differently in quantitative resistance of potato tubers to biotrophic and necrotrophic pathogens.
Identifieur interne : 001483 ( Main/Exploration ); précédent : 001482; suivant : 001484Nicotiflorin, rutin and chlorogenic acid: phenylpropanoids involved differently in quantitative resistance of potato tubers to biotrophic and necrotrophic pathogens.
Auteurs : Alexander Kröner [France] ; Nathalie Marnet ; Didier Andrivon ; Florence ValSource :
- Plant physiology and biochemistry : PPB [ 1873-2690 ] ; 2012.
Descripteurs français
- KwdFr :
- Acide chlorogénique (métabolisme), Flavonoïdes (métabolisme), Lipopolysaccharides (pharmacologie), Pectobacterium (composition chimique), Phytophthora infestans (pathogénicité), Phénols (métabolisme), Rutoside (métabolisme), Solanum tuberosum (effets des médicaments et des substances chimiques), Solanum tuberosum (métabolisme), Solanum tuberosum (parasitologie).
- MESH :
- composition chimique : Pectobacterium.
- effets des médicaments et des substances chimiques : Solanum tuberosum.
- métabolisme : Acide chlorogénique, Flavonoïdes, Phénols, Rutoside, Solanum tuberosum.
- parasitologie : Solanum tuberosum.
- pathogénicité : Phytophthora infestans.
- pharmacologie : Lipopolysaccharides.
English descriptors
- KwdEn :
- Chlorogenic Acid (metabolism), Flavonoids (metabolism), Lipopolysaccharides (pharmacology), Pectobacterium (chemistry), Phenols (metabolism), Phytophthora infestans (pathogenicity), Rutin (metabolism), Solanum tuberosum (drug effects), Solanum tuberosum (metabolism), Solanum tuberosum (parasitology).
- MESH :
- chemical , metabolism : Chlorogenic Acid, Flavonoids, Phenols, Rutin.
- chemical , pharmacology : Lipopolysaccharides.
- chemistry : Pectobacterium.
- drug effects : Solanum tuberosum.
- metabolism : Solanum tuberosum.
- parasitology : Solanum tuberosum.
- pathogenicity : Phytophthora infestans.
Abstract
Physiological and molecular mechanisms underlying quantitative resistance of plants to pathogens are still poorly understood, but could depend upon differences in the intensity or timing of general defense responses. This may be the case for the biosynthesis of phenolics which are known to increase after elicitation by pathogens. We thus tested the hypothesis that differences in quantitative resistance were related to differential induction of phenolics by pathogen-derived elicitors. Five potato cultivars (Solanum tuberosum, L.) spanning a range of quantitative resistance were treated with a concentrated culture filtrate (CCF) of Phytophthora infestans or purified lipopolysaccharides (LPS) from Pectobacterium atrosepticum. The kinetic of phenolics accumulation was followed and a set of typical phenolics was identified: chlorogenic acid, phenolamides and flavonols including rutin (quercetin-3-O-rutinoside) and nicotiflorin (kaempferol-3-O-rutinoside). Our results showed that CCF but not LPS induced differential accumulation of major phenolics among cultivars. Total phenolics were related with resistance to P. atrosepticum but not to P. infestans. However, nicotiflorin was inversely related with resistance to both pathogens. Rutin, but not nicotiflorin, inhibited pathogen growth in vitro at physiological concentrations. These data therefore suggest that (i) several phenolics are candidate markers for quantitative resistance in potato, (ii) some of these are pathogen specific although they are produced by a general defense pathway, (iii) resistance marker molecules do not necessarily have antimicrobial activity, and (iv) the final content of these target molecules-either constitutive or induced-is a better predictor of resistance than their inducibility by pathogen elicitors.
DOI: 10.1016/j.plaphy.2012.05.006
PubMed: 22677447
Affiliations:
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quantitative resistance of plants to pathogens are still poorly understood, but could depend upon differences in the intensity or timing of general defense responses. This may be the case for the biosynthesis of phenolics which are known to increase after elicitation by pathogens. We thus tested the hypothesis that differences in quantitative resistance were related to differential induction of phenolics by pathogen-derived elicitors. Five potato cultivars (Solanum tuberosum, L.) spanning a range of quantitative resistance were treated with a concentrated culture filtrate (CCF) of Phytophthora infestans or purified lipopolysaccharides (LPS) from Pectobacterium atrosepticum. The kinetic of phenolics accumulation was followed and a set of typical phenolics was identified: chlorogenic acid, phenolamides and flavonols including rutin (quercetin-3-O-rutinoside) and nicotiflorin (kaempferol-3-O-rutinoside). Our results showed that CCF but not LPS induced differential accumulation of major phenolics among cultivars. Total phenolics were related with resistance to P. atrosepticum but not to P. infestans. However, nicotiflorin was inversely related with resistance to both pathogens. Rutin, but not nicotiflorin, inhibited pathogen growth in vitro at physiological concentrations. These data therefore suggest that (i) several phenolics are candidate markers for quantitative resistance in potato, (ii) some of these are pathogen specific although they are produced by a general defense pathway, (iii) resistance marker molecules do not necessarily have antimicrobial activity, and (iv) the final content of these target molecules-either constitutive or induced-is a better predictor of resistance than their inducibility by pathogen elicitors.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22677447</PMID><DateCompleted><Year>2012</Year><Month>11</Month><Day>30</Day></DateCompleted><DateRevised><Year>2020</Year><Month>09</Month><Day>30</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-2690</ISSN><JournalIssue CitedMedium="Internet"><Volume>57</Volume><PubDate><Year>2012</Year><Month>Aug</Month></PubDate></JournalIssue><Title>Plant physiology and biochemistry : PPB</Title><ISOAbbreviation>Plant Physiol Biochem</ISOAbbreviation></Journal><ArticleTitle>Nicotiflorin, rutin and chlorogenic acid: phenylpropanoids involved differently in quantitative resistance of potato tubers to biotrophic and necrotrophic pathogens.</ArticleTitle><Pagination><MedlinePgn>23-31</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.plaphy.2012.05.006</ELocationID><Abstract><AbstractText>Physiological and molecular mechanisms underlying quantitative resistance of plants to pathogens are still poorly understood, but could depend upon differences in the intensity or timing of general defense responses. This may be the case for the biosynthesis of phenolics which are known to increase after elicitation by pathogens. We thus tested the hypothesis that differences in quantitative resistance were related to differential induction of phenolics by pathogen-derived elicitors. Five potato cultivars (Solanum tuberosum, L.) spanning a range of quantitative resistance were treated with a concentrated culture filtrate (CCF) of Phytophthora infestans or purified lipopolysaccharides (LPS) from Pectobacterium atrosepticum. The kinetic of phenolics accumulation was followed and a set of typical phenolics was identified: chlorogenic acid, phenolamides and flavonols including rutin (quercetin-3-O-rutinoside) and nicotiflorin (kaempferol-3-O-rutinoside). Our results showed that CCF but not LPS induced differential accumulation of major phenolics among cultivars. Total phenolics were related with resistance to P. atrosepticum but not to P. infestans. However, nicotiflorin was inversely related with resistance to both pathogens. Rutin, but not nicotiflorin, inhibited pathogen growth in vitro at physiological concentrations. These data therefore suggest that (i) several phenolics are candidate markers for quantitative resistance in potato, (ii) some of these are pathogen specific although they are produced by a general defense pathway, (iii) resistance marker molecules do not necessarily have antimicrobial activity, and (iv) the final content of these target molecules-either constitutive or induced-is a better predictor of resistance than their inducibility by pathogen elicitors.</AbstractText><CopyrightInformation>Copyright © 2012 Elsevier Masson SAS. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kröner</LastName><ForeName>Alexander</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Agrocampus Ouest, UMR1349 IGEPP, 35000 Rennes, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Marnet</LastName><ForeName>Nathalie</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Andrivon</LastName><ForeName>Didier</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Val</LastName><ForeName>Florence</ForeName><Initials>F</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2012</Year><Month>05</Month><Day>15</Day></ArticleDate></Article><MedlineJournalInfo><Country>France</Country><MedlineTA>Plant Physiol Biochem</MedlineTA><NlmUniqueID>9882449</NlmUniqueID><ISSNLinking>0981-9428</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005419">Flavonoids</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008070">Lipopolysaccharides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010636">Phenols</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C513882">nicotiflorin</NameOfSubstance></Chemical><Chemical><RegistryNumber>318ADP12RI</RegistryNumber><NameOfSubstance UI="D002726">Chlorogenic Acid</NameOfSubstance></Chemical><Chemical><RegistryNumber>5G06TVY3R7</RegistryNumber><NameOfSubstance UI="D012431">Rutin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D002726" MajorTopicYN="N">Chlorogenic 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PubStatus="pubmed"><Year>2012</Year><Month>6</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2012</Year><Month>12</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">22677447</ArticleId><ArticleId IdType="pii">S0981-9428(12)00111-8</ArticleId><ArticleId IdType="doi">10.1016/j.plaphy.2012.05.006</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li></country><region><li>Région Bretagne</li></region><settlement><li>Rennes</li></settlement></list><tree><noCountry><name sortKey="Andrivon, Didier" sort="Andrivon, Didier" uniqKey="Andrivon D" first="Didier" last="Andrivon">Didier Andrivon</name><name sortKey="Marnet, Nathalie" sort="Marnet, Nathalie" uniqKey="Marnet N" first="Nathalie" last="Marnet">Nathalie Marnet</name><name sortKey="Val, Florence" sort="Val, Florence" uniqKey="Val F" first="Florence" last="Val">Florence Val</name></noCountry><country name="France"><region name="Région Bretagne"><name sortKey="Kroner, Alexander" sort="Kroner, Alexander" uniqKey="Kroner A" first="Alexander" last="Kröner">Alexander Kröner</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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