Sequence diversity in the large subunit of RNA polymerase I contributes to Mefenoxam insensitivity in Phytophthora infestans.
Identifieur interne : 000F86 ( Main/Exploration ); précédent : 000F85; suivant : 000F87Sequence diversity in the large subunit of RNA polymerase I contributes to Mefenoxam insensitivity in Phytophthora infestans.
Auteurs : Eva Randall [Royaume-Uni] ; Vanessa Young ; Helge Sierotzki ; Gabriel Scalliet ; Paul R J. Birch ; David E L. Cooke ; Michael Csukai ; Stephen C. WhissonSource :
- Molecular plant pathology [ 1364-3703 ] ; 2014.
Descripteurs français
- KwdFr :
- Alanine (analogues et dérivés), Alanine (pharmacologie), Données de séquences moléculaires (MeSH), Phytophthora infestans (effets des médicaments et des substances chimiques), Phytophthora infestans (enzymologie), Phytophthora infestans (génétique), RNA polymerase I (composition chimique), RNA polymerase I (métabolisme), Résistance des champignons aux médicaments (MeSH).
- MESH :
- analogues et dérivés : Alanine.
- composition chimique : RNA polymerase I.
- effets des médicaments et des substances chimiques : Phytophthora infestans.
- enzymologie : Phytophthora infestans.
- génétique : Phytophthora infestans.
- métabolisme : RNA polymerase I.
- pharmacologie : Alanine.
- Données de séquences moléculaires, Résistance des champignons aux médicaments.
English descriptors
- KwdEn :
- MESH :
- chemical , analogs & derivatives : Alanine.
- chemical , chemistry : RNA Polymerase I.
- chemical , metabolism : RNA Polymerase I.
- chemical , pharmacology : Alanine.
- drug effects : Phytophthora infestans.
- enzymology : Phytophthora infestans.
- genetics : Phytophthora infestans.
- Drug Resistance, Fungal, Molecular Sequence Data.
Abstract
Phenylamide fungicides have been widely used for the control of oomycete-incited plant diseases for over 30 years. Insensitivity to this chemical class of fungicide was recorded early in its usage history, but the precise protein(s) conditioning insensitivity has proven difficult to determine. To determine the genetic basis of insensitivity and to inform strategies for the cloning of the gene(s) responsible, genetic crosses were established between Mefenoxam sensitive and intermediate insensitive isolates of Phytophthora infestans, the potato late blight pathogen. F1 progeny showed the expected semi-dominant phenotypes for Mefenoxam insensitivity and suggested the involvement of multiple loci, complicating the positional cloning of the gene(s) conditioning insensitivity to Mefenoxam. Instead, a candidate gene strategy was used, based on previous observations that the primary effect of phenylamide compounds is to inhibit ribosomal RNA synthesis. The subunits of RNA polymerase I (RNApolI) were sequenced from sensitive and insensitive isolates and F1 progeny. Single nucleotide polymorphisms (SNPs) specific to insensitive field isolates were identified in the gene encoding the large subunit of RNApolI. In a survey of field isolates, SNP T1145A (Y382F) showed an 86% association with Mefenoxam insensitivity. Isolates not showing this association belonged predominantly to one P. infestans genotype. The transfer of the 'insensitive' allele of RPA190 to a sensitive isolate yielded transgenic lines that were insensitive to Mefenoxam. These results demonstrate that sequence variation in RPA190 contributes to insensitivity to Mefenoxam in P. infestans.
DOI: 10.1111/mpp.12124
PubMed: 24521429
PubMed Central: PMC6638662
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Insensitivity to this chemical class of fungicide was recorded early in its usage history, but the precise protein(s) conditioning insensitivity has proven difficult to determine. To determine the genetic basis of insensitivity and to inform strategies for the cloning of the gene(s) responsible, genetic crosses were established between Mefenoxam sensitive and intermediate insensitive isolates of Phytophthora infestans, the potato late blight pathogen. F1 progeny showed the expected semi-dominant phenotypes for Mefenoxam insensitivity and suggested the involvement of multiple loci, complicating the positional cloning of the gene(s) conditioning insensitivity to Mefenoxam. Instead, a candidate gene strategy was used, based on previous observations that the primary effect of phenylamide compounds is to inhibit ribosomal RNA synthesis. The subunits of RNA polymerase I (RNApolI) were sequenced from sensitive and insensitive isolates and F1 progeny. Single nucleotide polymorphisms (SNPs) specific to insensitive field isolates were identified in the gene encoding the large subunit of RNApolI. In a survey of field isolates, SNP T1145A (Y382F) showed an 86% association with Mefenoxam insensitivity. Isolates not showing this association belonged predominantly to one P. infestans genotype. The transfer of the 'insensitive' allele of RPA190 to a sensitive isolate yielded transgenic lines that were insensitive to Mefenoxam. These results demonstrate that sequence variation in RPA190 contributes to insensitivity to Mefenoxam in P. infestans. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24521429</PMID><DateCompleted><Year>2015</Year><Month>04</Month><Day>15</Day></DateCompleted><DateRevised><Year>2020</Year><Month>02</Month><Day>25</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1364-3703</ISSN><JournalIssue CitedMedium="Internet"><Volume>15</Volume><Issue>7</Issue><PubDate><Year>2014</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Molecular plant pathology</Title><ISOAbbreviation>Mol Plant Pathol</ISOAbbreviation></Journal><ArticleTitle>Sequence diversity in the large subunit of RNA polymerase I contributes to Mefenoxam insensitivity in Phytophthora infestans.</ArticleTitle><Pagination><MedlinePgn>664-76</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/mpp.12124</ELocationID><Abstract><AbstractText>Phenylamide fungicides have been widely used for the control of oomycete-incited plant diseases for over 30 years. Insensitivity to this chemical class of fungicide was recorded early in its usage history, but the precise protein(s) conditioning insensitivity has proven difficult to determine. To determine the genetic basis of insensitivity and to inform strategies for the cloning of the gene(s) responsible, genetic crosses were established between Mefenoxam sensitive and intermediate insensitive isolates of Phytophthora infestans, the potato late blight pathogen. F1 progeny showed the expected semi-dominant phenotypes for Mefenoxam insensitivity and suggested the involvement of multiple loci, complicating the positional cloning of the gene(s) conditioning insensitivity to Mefenoxam. Instead, a candidate gene strategy was used, based on previous observations that the primary effect of phenylamide compounds is to inhibit ribosomal RNA synthesis. The subunits of RNA polymerase I (RNApolI) were sequenced from sensitive and insensitive isolates and F1 progeny. Single nucleotide polymorphisms (SNPs) specific to insensitive field isolates were identified in the gene encoding the large subunit of RNApolI. In a survey of field isolates, SNP T1145A (Y382F) showed an 86% association with Mefenoxam insensitivity. Isolates not showing this association belonged predominantly to one P. infestans genotype. The transfer of the 'insensitive' allele of RPA190 to a sensitive isolate yielded transgenic lines that were insensitive to Mefenoxam. These results demonstrate that sequence variation in RPA190 contributes to insensitivity to Mefenoxam in P. infestans. </AbstractText><CopyrightInformation>© 2014 BSPP AND JOHN WILEY & SONS LTD.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Randall</LastName><ForeName>Eva</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Cell and Molecular Sciences, James Hutton Institute, Invergowrie, Dundee, DD2 5DA, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Young</LastName><ForeName>Vanessa</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Sierotzki</LastName><ForeName>Helge</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Scalliet</LastName><ForeName>Gabriel</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Birch</LastName><ForeName>Paul R J</ForeName><Initials>PR</Initials></Author><Author ValidYN="Y"><LastName>Cooke</LastName><ForeName>David E L</ForeName><Initials>DE</Initials></Author><Author ValidYN="Y"><LastName>Csukai</LastName><ForeName>Michael</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Whisson</LastName><ForeName>Stephen C</ForeName><Initials>SC</Initials></Author></AuthorList><Language>eng</Language><DataBankList CompleteYN="Y"><DataBank><DataBankName>GENBANK</DataBankName><AccessionNumberList><AccessionNumber>AAA33749</AccessionNumber><AccessionNumber>EEY66296</AccessionNumber><AccessionNumber>EU257520</AccessionNumber></AccessionNumberList></DataBank></DataBankList><GrantList CompleteYN="Y"><Grant><GrantID>BB/E007120/1</GrantID><Agency>Biotechnology and Biological Sciences Research Council</Agency><Country>United Kingdom</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>04</Month><Day>14</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Mol Plant Pathol</MedlineTA><NlmUniqueID>100954969</NlmUniqueID><ISSNLinking>1364-3703</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>EC 2.7.7.6</RegistryNumber><NameOfSubstance UI="D012318">RNA Polymerase I</NameOfSubstance></Chemical><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><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D025141" MajorTopicYN="N">Drug Resistance, Fungal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008969" MajorTopicYN="N">Molecular Sequence Data</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055750" MajorTopicYN="N">Phytophthora infestans</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012318" MajorTopicYN="N">RNA Polymerase I</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Mefenoxam</Keyword><Keyword MajorTopicYN="N">Metalaxyl</Keyword><Keyword MajorTopicYN="N">Phytophthora infestans</Keyword><Keyword MajorTopicYN="N">RNA polymerase</Keyword><Keyword MajorTopicYN="N">fungicide</Keyword><Keyword MajorTopicYN="N">oomycete</Keyword><Keyword MajorTopicYN="N">phenylamide</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>2</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>2</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>4</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">24521429</ArticleId><ArticleId IdType="doi">10.1111/mpp.12124</ArticleId><ArticleId IdType="pmc">PMC6638662</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Fungal Genet Biol. 1999 Mar;26(2):118-30</Citation><ArticleIdList><ArticleId 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Birch</name><name sortKey="Cooke, David E L" sort="Cooke, David E L" uniqKey="Cooke D" first="David E L" last="Cooke">David E L. Cooke</name><name sortKey="Csukai, Michael" sort="Csukai, Michael" uniqKey="Csukai M" first="Michael" last="Csukai">Michael Csukai</name><name sortKey="Scalliet, Gabriel" sort="Scalliet, Gabriel" uniqKey="Scalliet G" first="Gabriel" last="Scalliet">Gabriel Scalliet</name><name sortKey="Sierotzki, Helge" sort="Sierotzki, Helge" uniqKey="Sierotzki H" first="Helge" last="Sierotzki">Helge Sierotzki</name><name sortKey="Whisson, Stephen C" sort="Whisson, Stephen C" uniqKey="Whisson S" first="Stephen C" last="Whisson">Stephen C. Whisson</name><name sortKey="Young, Vanessa" sort="Young, Vanessa" uniqKey="Young V" first="Vanessa" last="Young">Vanessa Young</name></noCountry><country name="Royaume-Uni"><noRegion><name sortKey="Randall, Eva" sort="Randall, Eva" uniqKey="Randall E" first="Eva" last="Randall">Eva Randall</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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