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 |