Abstract

BACKGROUNDMetyltetraprole is a novel quinol oxidation site of Complex III inhibitor (QoI) fungicide that inhibits mitochondrial electron transport at the Qo site of the cytochrome bc1 complex. Previous reports have demonstrated that it is also active against the QoI‐resistant (QoI‐R) isolates of Zymoseptoria tritici and Pyrenophora teres with the mutations G143A and F129L in their cytochrome b gene, respectively. Further studies on cross‐resistance between metyltetraprole and existing QoIs were performed using an increased number of isolates of Z. tritici, P. teres, Ramularia collo‐cygni, Pyrenophora tritici‐repentis, and several other plant pathogenic fungi.RESULTSDifferences in the EC50 values between the wild‐type and QoI‐R isolates with the mutations G143A or F129L were always smaller for metyltetraprole compared to those for the existing QoIs, and they were never greater than five in terms of resistance factor. The 2‐year field experiments showed that the metyltetraprole treatment did not increase the percentage of QoI‐R isolates likely to harbor the G143A mutation in a Z. tritici population.CONCLUSIONThe unique behavior of metyltetraprole against the existing QoI‐R isolates was confirmed for all tested pathogen species. Our results provide important information to establish a fungicide resistance management strategy using metyltetraprole in combination or alternation with other fungicides. © 2019 The Authors. Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.

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