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Molecular characterization of benzimidazole-resistant B. cinerea field isolates with reduced or enhanced sensitivity to zoxamide and diethofencarb

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dc.contributor.author Malandrakis, A en
dc.contributor.author Markoglou, A en
dc.contributor.author Ziogas, B en
dc.date.accessioned 2014-06-06T06:51:23Z
dc.date.available 2014-06-06T06:51:23Z
dc.date.issued 2011 en
dc.identifier.issn 00483575 en
dc.identifier.uri http://dx.doi.org/10.1016/j.pestbp.2010.11.008 en
dc.identifier.uri http://62.217.125.90/xmlui/handle/123456789/5485
dc.subject β-Tubulin mutations en
dc.subject Diethofencarb sensitivity en
dc.subject Molecular diagnostic en
dc.subject Monitoring resistance en
dc.subject Zoxamide resistance en
dc.subject.other Botryotinia fuckeliana en
dc.title Molecular characterization of benzimidazole-resistant B. cinerea field isolates with reduced or enhanced sensitivity to zoxamide and diethofencarb en
heal.type journalArticle en
heal.identifier.primary 10.1016/j.pestbp.2010.11.008 en
heal.publicationDate 2011 en
heal.abstract Sensitivity profiles of Botrytis cinerea field isolates to zoxamide and the molecular basis of the resistance mechanism involved in cross-resistance relationships between benzamides, benzimidazoles and N-phenylcarbamates were investigated. B. cinerea isolates collected from southern, central and northern Greece were characterized based on their sensitivity to zoxamide, the benzimidazole carbendazim and the N-phenylcarbamate diethofencarb. Isolates exhibiting baseline sensitivity to carbendazim and zoxamide but no sensitivity to diethofencarb were considered wild type (S phenotype) and accounted for 44% of the total strains sampled. Thirty-three percent of the isolates had increased sensitivity (HS phenotype) to zoxamide and diethofencarb and were highly resistant to carbendazim compared to S isolates. Eight percent of the sample was highly resistant (HR phenotype) to all anti-tubulin agents studied. The rest of the isolates were moderately resistant to zoxamide (MR phenotype) and equally sensitive to benzimidazoles and N-phenylcarbamates compared to isolates of the S phenotype. Fungitoxicity tests with botrycides belonging to other chemical classes revealed no cross-resistance relationships between zoxamide and the phenylpyrrole fludioxonil, the dicarboximide iprodione, the hydroxyanilide fenhexamid, the anilinopyrimidine cyprodinil, the carboxamide boscalid and the strobilurin-type fungicide pyraclostrobin. Study of fitness characteristics did not show any significant difference between zoxamide resistant and sensitive isolates with respect to the parameters tested. PCR-RFLP analysis of a part of the β-tubulin gene sequence detected mutations in position 198 for both HS and HR zoxamide-sensitivity phenotypes. DNA sequence analysis of the B. cinerea β-tubulin gene revealed two previously described benzimidazole-resistance-conferring mutations. The first one was the glutamic acid (GAG) to alanine (GCG) change at position 198 (E198A), which was identified in all HS isolates. The second mutation (E198K) was a GAG-to-AAG substitution resulting in the replacement of glutamic acid with lysine present in all B. cinerea isolates highly resistant to all three anti-tubulin classes of fungicides. A number of mutations in other positions of the β-tubulin gene were detected in the moderately zoxamide-resistance phenotype. © 2010 Elsevier Inc. en
heal.journalName Pesticide Biochemistry and Physiology en
dc.identifier.issue 1 en
dc.identifier.volume 99 en
dc.identifier.doi 10.1016/j.pestbp.2010.11.008 en
dc.identifier.spage 118 en
dc.identifier.epage 124 en


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