Genetic control of resistance to fenpropimorph in Ustilago maydis

Fenpropimorph‐resistant mutants of Ustilago maydis were obtained at high frequency (30 × 10 −6 ) after UV‐irradiation followed by selection on media containing fenpropimorph (50 μ g mL −1 ). Genetic analysis of 30 such mutants resulted in the identification of two unlinked chromosomal loci, the U/fpm ‐1 locus with two allelic genes ( U/fpm‐ 1A and U/fpm ‐1B) and the U/fpm ‐2 locus. The mutant genes U/fpm‐ 1A and U/fpm ‐2 are responsible for high resistance levels (Rf: 75–100 or 257–286 based on MICs or ED 50s , respectively), while the U/fpm ‐1B mutation gives only a small reduction (approximately 7–10‐fold) in fenpropimorph sensitivity. Cross‐resistance studies with other SBIs showed that the major gene ( U/fpm‐ 1A and U/fpm ‐2) mutants were cross‐resistant to the related compound fenpropidin (Rf: 15–20 or 53–66 based on MICs or ED 50s values, respectively) and to tridemorph (Rf: 5 or 7.1–9.5 based on MICs or ED 50s values, respectively), but not to the inhibitors of steps of ergosterol biosynthesis preceding the Δ 14 ‐reductase. The minor gene ( U/fpm ‐1B) mutants also had low‐level resistance (approximately 5‐fold) to tridemorph and to fenpropidin, but in contrast with the major gene mutants they were 2–10 times more sensitive to the triazoles studied (triadimefon, triadimenol, propiconazole and flusilazole) and to the pyridine, pyrifenox. Studies of the fitness of U. maydis mutants showed that in major gene mutants, resistance was not associated with changes in growth rate in liquid culture or pathogenicity on young maize plants. The minor gene mutation reduced significantly the growth rate in liquid culture and the pathogenicity, either in homozygous or heterozygous condition in dikaryotic mycelium.