Evolution of fungicide resistance in UK field populations of Zymoseptoria tritici
Bart Fraaije: Rothamsted Research
<div>The fungal wheat pathogen<em> Zymoseptoria tritici</em> is becoming more difficult to control in NW-Europe. Using archived infected wheat leaf samples from Broadbalk, the long-term winter wheat experiment at Rothamsted, resistance to methyl benzimidazole carbamates and quinone outside inhibitors due to alterations in β-tubulin (E198A) and cytochrome <em>b</em> (G143A) was detected in 1985 and 2002, respectively. UK field populations have also become less sensitive to azoles due to three different mechanisms, alterations in the target protein sterol 14α-demethylase (CYP51) with the first mutation, Y137F, detected in 1991, CYP51 over-expression (2009) and altered efflux pump activity (2013). All three mechanisms have been found simultaneously in some isolates. Resistance conferring mutations to succinate dehydrogenase inhibitors (SDHIs) have also been detected since 2015, with up to 15 different mutations found in <em>SdhB</em>, <em>SdhC</em> and <em>SdhD</em> in 2017. Two isolates carried two mutations simultaneously, but these strains were not found in subsequent years. Here we present the latest monitoring data from the four most frequently occurring Sdh mutations (SdhC-T79N, C-W80S, C-N86S and C-H152R) in the UK at the start of the season in different geographical regions and late season after selection by different fungicide programmes. Previous studies and results from our current monitoring studies indicate that isolates carrying C-H152R might harbour a fitness cost. Quantitative detection of the four targeted <em>Sdh</em> mutations show that selection for these mutations was influenced by the dose rate, spray number and mixing partner of SDHI fungicides.</div>
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