C239S Mutation in the β-Tubulin of Phytophthora sojae Confers Resistance to Zoxamide.
Identifieur interne : 000B93 ( Main/Curation ); précédent : 000B92; suivant : 000B94C239S Mutation in the β-Tubulin of Phytophthora sojae Confers Resistance to Zoxamide.
Auteurs : Meng Cai [États-Unis] ; Jianqiang Miao [République populaire de Chine] ; Xi Song [République populaire de Chine] ; Dong Lin [République populaire de Chine] ; Yang Bi [République populaire de Chine] ; Lei Chen [République populaire de Chine] ; Xili Liu [République populaire de Chine] ; Brett M. Tyler [États-Unis]Source :
- Frontiers in microbiology [ 1664-302X ] ; 2016.
Abstract
Zoxamide is the sole β-tubulin inhibitor registered for the control of oomycete pathogens. The current study investigated the activity of zoxamide against Phytophthora sojae and baseline sensitivity was established with a mean EC50 of 0.048 μg/ml. The data is critical for monitoring changes in zoxamide-sensitivity in the field. Three stable resistant mutants with a high resistance level were obtained by selection on zoxamide amended media. Although the development of resistance occurred at a low frequency, there were no apparent fitness penalty in the acquired mutants in terms of growth rate, sporulation, germination and pathogenicity. Based on the biological profiles and low mutagenesis rate, the resistance risk of P. sojae to zoxamide can be estimated as low to medium. Further investigation revealed all the zoxamide-resistant mutants had a point mutation of C239S in their β-tubulin. Zoxamide also exhibited high activity against most species from the genus Pythium in which only Pythium aphanidermatum was found naturally resistant to zoxamide and harboring the natural point mutation S239 in the β-tubulin. Back-transformation in P. sojae with the mutated allele (S239) confirmed the C239S mutation can induce resistance to zoxamide, and the resistance level was positively related to the expression level of the mutated gene. In contrast, the overexpression of the wild type gene was unable to cause zoxamide resistance. It is the first report on the resistance molecular mechanism of zoxamide in oomycetes. Based on our study, C239 is supposed to be a key target site of zoxamide, which distinguishes zoxamide from benzimidazoles and accounts for its low resistance risk. The result can provide advice on the design of new β-tubulin inhibitors in future.
DOI: 10.3389/fmicb.2016.00762
PubMed: 27242773
PubMed Central: PMC4873504
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Tyler</name><affiliation wicri:level="1"><nlm:affiliation>Department of Botany and Plant Pathology, Oregon State University, Corvallis OR, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Botany and Plant Pathology, Oregon State University, Corvallis OR</wicri:regionArea></affiliation></author></analytic><series><title level="j">Frontiers in microbiology</title><idno type="ISSN">1664-302X</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Zoxamide is the sole β-tubulin inhibitor registered for the control of oomycete pathogens. The current study investigated the activity of zoxamide against Phytophthora sojae and baseline sensitivity was established with a mean EC50 of 0.048 μg/ml. The data is critical for monitoring changes in zoxamide-sensitivity in the field. Three stable resistant mutants with a high resistance level were obtained by selection on zoxamide amended media. Although the development of resistance occurred at a low frequency, there were no apparent fitness penalty in the acquired mutants in terms of growth rate, sporulation, germination and pathogenicity. Based on the biological profiles and low mutagenesis rate, the resistance risk of P. sojae to zoxamide can be estimated as low to medium. Further investigation revealed all the zoxamide-resistant mutants had a point mutation of C239S in their β-tubulin. Zoxamide also exhibited high activity against most species from the genus Pythium in which only Pythium aphanidermatum was found naturally resistant to zoxamide and harboring the natural point mutation S239 in the β-tubulin. Back-transformation in P. sojae with the mutated allele (S239) confirmed the C239S mutation can induce resistance to zoxamide, and the resistance level was positively related to the expression level of the mutated gene. In contrast, the overexpression of the wild type gene was unable to cause zoxamide resistance. It is the first report on the resistance molecular mechanism of zoxamide in oomycetes. Based on our study, C239 is supposed to be a key target site of zoxamide, which distinguishes zoxamide from benzimidazoles and accounts for its low resistance risk. The result can provide advice on the design of new β-tubulin inhibitors in future. </div></front></TEI><pubmed><MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM"><PMID Version="1">27242773</PMID><DateCompleted><Year>2016</Year><Month>05</Month><Day>31</Day></DateCompleted><DateRevised><Year>2020</Year><Month>09</Month><Day>29</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Print">1664-302X</ISSN><JournalIssue CitedMedium="Print"><Volume>7</Volume><PubDate><Year>2016</Year></PubDate></JournalIssue><Title>Frontiers in microbiology</Title><ISOAbbreviation>Front Microbiol</ISOAbbreviation></Journal><ArticleTitle>C239S Mutation in the β-Tubulin of Phytophthora sojae Confers Resistance to Zoxamide.</ArticleTitle><Pagination><MedlinePgn>762</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3389/fmicb.2016.00762</ELocationID><Abstract><AbstractText>Zoxamide is the sole β-tubulin inhibitor registered for the control of oomycete pathogens. The current study investigated the activity of zoxamide against Phytophthora sojae and baseline sensitivity was established with a mean EC50 of 0.048 μg/ml. The data is critical for monitoring changes in zoxamide-sensitivity in the field. Three stable resistant mutants with a high resistance level were obtained by selection on zoxamide amended media. Although the development of resistance occurred at a low frequency, there were no apparent fitness penalty in the acquired mutants in terms of growth rate, sporulation, germination and pathogenicity. Based on the biological profiles and low mutagenesis rate, the resistance risk of P. sojae to zoxamide can be estimated as low to medium. Further investigation revealed all the zoxamide-resistant mutants had a point mutation of C239S in their β-tubulin. Zoxamide also exhibited high activity against most species from the genus Pythium in which only Pythium aphanidermatum was found naturally resistant to zoxamide and harboring the natural point mutation S239 in the β-tubulin. Back-transformation in P. sojae with the mutated allele (S239) confirmed the C239S mutation can induce resistance to zoxamide, and the resistance level was positively related to the expression level of the mutated gene. In contrast, the overexpression of the wild type gene was unable to cause zoxamide resistance. It is the first report on the resistance molecular mechanism of zoxamide in oomycetes. Based on our study, C239 is supposed to be a key target site of zoxamide, which distinguishes zoxamide from benzimidazoles and accounts for its low resistance risk. The result can provide advice on the design of new β-tubulin inhibitors in future. </AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Cai</LastName><ForeName>Meng</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Plant Pathology, China Agricultural UniversityBeijing, China; Department of Botany and Plant Pathology, Oregon State University, CorvallisOR, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Miao</LastName><ForeName>Jianqiang</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Plant Pathology, China Agricultural University Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Song</LastName><ForeName>Xi</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Plant Pathology, China Agricultural University Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lin</LastName><ForeName>Dong</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Plant Pathology, China Agricultural University Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bi</LastName><ForeName>Yang</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Plant Science and Technology College, Beijing University of Agriculture Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Lei</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>College of Forestry, Beijing Forestry University Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Xili</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Plant Pathology, China Agricultural University Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tyler</LastName><ForeName>Brett M</ForeName><Initials>BM</Initials><AffiliationInfo><Affiliation>Department of Botany and Plant Pathology, Oregon State University, Corvallis OR, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>05</Month><Day>20</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Microbiol</MedlineTA><NlmUniqueID>101548977</NlmUniqueID><ISSNLinking>1664-302X</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">C239S</Keyword><Keyword MajorTopicYN="N">molecular mechanism of resistance</Keyword><Keyword MajorTopicYN="N">oomycetes</Keyword><Keyword MajorTopicYN="N">resistance risk</Keyword><Keyword MajorTopicYN="N">zoxamide</Keyword><Keyword MajorTopicYN="N">β-tubulin inhibitor</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>03</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>05</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>6</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>6</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>6</Month><Day>1</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27242773</ArticleId><ArticleId IdType="doi">10.3389/fmicb.2016.00762</ArticleId><ArticleId IdType="pmc">PMC4873504</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Trends Microbiol. 2008 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