Acquired Resistance to Mefenoxam in Sensitive Isolates of Phytophthora infestans.
Identifieur interne : 000F33 ( Main/Exploration ); précédent : 000F32; suivant : 000F34Acquired Resistance to Mefenoxam in Sensitive Isolates of Phytophthora infestans.
Auteurs : Richard Childers ; Giovanna Danies ; Kevin Myers ; Zhangjun Fei ; Ian M. Small ; William E. FrySource :
- Phytopathology [ 0031-949X ] ; 2015.
Descripteurs français
- KwdFr :
- MESH :
- analogues et dérivés : Alanine.
- physiologie : Phytophthora infestans.
- Analyse de séquence d'ADN, Génotype, Résistance microbienne aux médicaments, Transcriptome.
English descriptors
- KwdEn :
- MESH :
- chemical , analogs & derivatives : Alanine.
- physiology : Phytophthora infestans.
- Drug Resistance, Microbial, Genotype, Sequence Analysis, DNA, Transcriptome.
Abstract
The systemic fungicide mefenoxam has been important in the control of late blight disease caused by Phytophthora infestans. This phenylamide fungicide has a negative effect on the synthesis of ribosomal RNA; however, the genetic basis for inherited field resistance is still not completely clear. We recently observed that a sensitive isolate became tolerant after a single passage on mefenoxam-containing medium. Further analyses revealed that all sensitive isolates tested (in three diverse genotypes) acquired this resistance equally quickly. In contrast, isolates that were "resistant" to mefenoxam in the initial assessment (stably resistant) did not increase in resistance upon further exposure. However, there appeared to be a cost associated with acquired resistance in the initially sensitive isolates, in that isolates with acquired resistance grew more slowly on mefenoxam-free medium than did the same isolates that had never been exposed to mefenoxam. The acquired resistance of the sensitive isolates declined slightly with subsequent culturing on medium free of mefenoxam. To investigate the mechanism of acquired resistance, we employed strand-specific RNA sequencing. Many differentially expressed genes were genotype specific, but one set of genes was differentially expressed in all genotypes. Among these were several genes (a phospholipase "Pi-PLD-like-3," two ATP-binding cassette superfamily [ABC] transporters, and a mannitol dehydrogenase) that were up-regulated and whose function might contribute to a resistance phenotype.
DOI: 10.1094/PHYTO-05-14-0148-R
PubMed: 25226526
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Fry</name></author></analytic><series><title level="j">Phytopathology</title><idno type="ISSN">0031-949X</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Alanine (analogs & derivatives)</term><term>Drug Resistance, Microbial (MeSH)</term><term>Genotype (MeSH)</term><term>Phytophthora infestans (physiology)</term><term>Sequence Analysis, DNA (MeSH)</term><term>Transcriptome (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Alanine (analogues et dérivés)</term><term>Analyse de séquence d'ADN (MeSH)</term><term>Génotype (MeSH)</term><term>Phytophthora infestans (physiologie)</term><term>Résistance microbienne aux médicaments (MeSH)</term><term>Transcriptome (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Alanine</term></keywords><keywords scheme="MESH" qualifier="analogues et dérivés" xml:lang="fr"><term>Alanine</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Phytophthora infestans</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Phytophthora infestans</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Drug Resistance, Microbial</term><term>Genotype</term><term>Sequence Analysis, DNA</term><term>Transcriptome</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Analyse de séquence d'ADN</term><term>Génotype</term><term>Résistance microbienne aux médicaments</term><term>Transcriptome</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The systemic fungicide mefenoxam has been important in the control of late blight disease caused by Phytophthora infestans. This phenylamide fungicide has a negative effect on the synthesis of ribosomal RNA; however, the genetic basis for inherited field resistance is still not completely clear. We recently observed that a sensitive isolate became tolerant after a single passage on mefenoxam-containing medium. Further analyses revealed that all sensitive isolates tested (in three diverse genotypes) acquired this resistance equally quickly. In contrast, isolates that were "resistant" to mefenoxam in the initial assessment (stably resistant) did not increase in resistance upon further exposure. However, there appeared to be a cost associated with acquired resistance in the initially sensitive isolates, in that isolates with acquired resistance grew more slowly on mefenoxam-free medium than did the same isolates that had never been exposed to mefenoxam. The acquired resistance of the sensitive isolates declined slightly with subsequent culturing on medium free of mefenoxam. To investigate the mechanism of acquired resistance, we employed strand-specific RNA sequencing. Many differentially expressed genes were genotype specific, but one set of genes was differentially expressed in all genotypes. Among these were several genes (a phospholipase "Pi-PLD-like-3," two ATP-binding cassette superfamily [ABC] transporters, and a mannitol dehydrogenase) that were up-regulated and whose function might contribute to a resistance phenotype. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25226526</PMID><DateCompleted><Year>2015</Year><Month>11</Month><Day>06</Day></DateCompleted><DateRevised><Year>2015</Year><Month>02</Month><Day>18</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0031-949X</ISSN><JournalIssue CitedMedium="Print"><Volume>105</Volume><Issue>3</Issue><PubDate><Year>2015</Year><Month>Mar</Month></PubDate></JournalIssue><Title>Phytopathology</Title><ISOAbbreviation>Phytopathology</ISOAbbreviation></Journal><ArticleTitle>Acquired Resistance to Mefenoxam in Sensitive Isolates of Phytophthora infestans.</ArticleTitle><Pagination><MedlinePgn>342-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1094/PHYTO-05-14-0148-R</ELocationID><Abstract><AbstractText>The systemic fungicide mefenoxam has been important in the control of late blight disease caused by Phytophthora infestans. This phenylamide fungicide has a negative effect on the synthesis of ribosomal RNA; however, the genetic basis for inherited field resistance is still not completely clear. We recently observed that a sensitive isolate became tolerant after a single passage on mefenoxam-containing medium. Further analyses revealed that all sensitive isolates tested (in three diverse genotypes) acquired this resistance equally quickly. In contrast, isolates that were "resistant" to mefenoxam in the initial assessment (stably resistant) did not increase in resistance upon further exposure. However, there appeared to be a cost associated with acquired resistance in the initially sensitive isolates, in that isolates with acquired resistance grew more slowly on mefenoxam-free medium than did the same isolates that had never been exposed to mefenoxam. The acquired resistance of the sensitive isolates declined slightly with subsequent culturing on medium free of mefenoxam. To investigate the mechanism of acquired resistance, we employed strand-specific RNA sequencing. Many differentially expressed genes were genotype specific, but one set of genes was differentially expressed in all genotypes. Among these were several genes (a phospholipase "Pi-PLD-like-3," two ATP-binding cassette superfamily [ABC] transporters, and a mannitol dehydrogenase) that were up-regulated and whose function might contribute to a resistance phenotype. </AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Childers</LastName><ForeName>Richard</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Danies</LastName><ForeName>Giovanna</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Myers</LastName><ForeName>Kevin</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Fei</LastName><ForeName>Zhangjun</ForeName><Initials>Z</Initials></Author><Author ValidYN="Y"><LastName>Small</LastName><ForeName>Ian M</ForeName><Initials>IM</Initials></Author><Author ValidYN="Y"><LastName>Fry</LastName><ForeName>William E</ForeName><Initials>WE</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></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Phytopathology</MedlineTA><NlmUniqueID>9427222</NlmUniqueID><ISSNLinking>0031-949X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>F1Q54ONN4H</RegistryNumber><NameOfSubstance UI="C473256">mefenoxam</NameOfSubstance></Chemical><Chemical><RegistryNumber>OF5P57N2ZX</RegistryNumber><NameOfSubstance UI="D000409">Alanine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000409" MajorTopicYN="N">Alanine</DescriptorName><QualifierName UI="Q000031" MajorTopicYN="Y">analogs & derivatives</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004352" MajorTopicYN="Y">Drug Resistance, Microbial</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005838" MajorTopicYN="N">Genotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055750" MajorTopicYN="N">Phytophthora infestans</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017422" MajorTopicYN="N">Sequence Analysis, DNA</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D059467" MajorTopicYN="N">Transcriptome</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>9</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>9</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>11</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">25226526</ArticleId><ArticleId IdType="doi">10.1094/PHYTO-05-14-0148-R</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list></list><tree><noCountry><name sortKey="Childers, Richard" sort="Childers, Richard" uniqKey="Childers R" first="Richard" last="Childers">Richard Childers</name><name sortKey="Danies, Giovanna" sort="Danies, Giovanna" uniqKey="Danies G" first="Giovanna" last="Danies">Giovanna Danies</name><name sortKey="Fei, Zhangjun" sort="Fei, Zhangjun" uniqKey="Fei Z" first="Zhangjun" last="Fei">Zhangjun Fei</name><name sortKey="Fry, William E" sort="Fry, William E" uniqKey="Fry W" first="William E" last="Fry">William E. Fry</name><name sortKey="Myers, Kevin" sort="Myers, Kevin" uniqKey="Myers K" first="Kevin" last="Myers">Kevin Myers</name><name sortKey="Small, Ian M" sort="Small, Ian M" uniqKey="Small I" first="Ian M" last="Small">Ian M. Small</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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