期刊
PEST MANAGEMENT SCIENCE
卷 75, 期 8, 页码 2107-2114出版社
JOHN WILEY & SONS LTD
DOI: 10.1002/ps.5264
关键词
QiI; bc(1) complex; yeast model; resistance; target site mutation; fungicides
资金
- ANSES (French Agency for Food, Environmental and Occupational Health Safety)
- Photosynthetic Systems program from Division of Chemical Sciences, Geosciences, and Biosciences, Office of Basic Energy Sciences of the U.S. Department of Energy [DE-FG02-11ER16220]
BACKGROUND Complex III inhibitors targeting the Q(i)-site have been known for decades; some are used or being developed as antimicrobial compounds. Target site resistance mutations have been reported in laboratory-selected mutants and in field isolates. Here, we present a brief overview of mutations found in laboratory-selected resistant mutants. We also provide a study of mutations observed in field isolates of Plasmopara viticola, in particular the ametoctradin resistance substitution, S34L that we analysed in the yeast model. RESULTS A survey of laboratory mutants showed that resistance could be caused by a large number of substitutions in the Q(i)-site. Four residues seemed key in term of resistance: N31, G37, L198 and K228. Using yeast, we analysed the effect of the ametoctradin resistance substitution S34L reported in field isolates of P. viticola. We showed that S34L caused a high level of resistance combined with a loss of complex III activity and growth competence. CONCLUSION Use of single site Q(i)-site inhibitors is expected to result in the selection of resistant mutants. However, if the substitution is associated with a fitness penalty, as may be the case with S34L, resistance development might not be an insuperable obstacle, although careful monitoring is required. (c) 2018 Society of Chemical Industry
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