Just one at a time: fungal population experiments with Zymoseptoria tritici and metyltetraprole (Pavecto®) demonstrate the incompatibility of different cytochrome B mutations

Abstract

The complex III of the mitochondrial respiration chain is an effective fungicidal target in plant pathogenic fungi. Especially the QoIs (FRAC Group 11 and 11A) fungicides cover a broad pathogen spectrum, that includes ascomycetes, basidiomycetes and oomycetes, by inhibiting the complex III at the outer binding site. Many of the target pathogens have developed resistance mediated by the target site mutation G143A. All fungicides that belong to Group 11 are affected by this mutation. Metyltetraprole has been recently developed, and it also binds at the Qo-site but is not affected by the G143A mutation and has therefore been classified differently (FRAC Group 11A). In experiments on solid medium with sequential exposure to complex III inhibitors, laboratory mutants of Zymoseptoria tritici with a resistance to metyltetraprole could be selected. Resistance to metyltetraprole was mediated by the target site mutation in the cytochrome B gene leading to the aa change Y132C. Metyltetraprole resistant isolates could only be generated from wildtype parents, but not from G143A parents. Further experiments used serial batch cultivations in liquid media with increasing fungicide concentrations. These were aimed to select double mutants that harboured both G143A and Y132C. Several different parental strains were treated with increasing concentrations of metyltetraprole, but no Y132C mutants were found when G143A parents were used. When Y132C mutants were used as the initial inoculum, and these were exposed to increasing concentrations of pyraclostrobin, the parental mutation was replaced by G143A within a few cycles; this could suggest that both mutations are incompatible.