The Y123H substitution perturbs Fv CYP 51B function and confers prochloraz resistance in laboratory mutants of F usarium verticillioides

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Abstract
Fusarium verticillioides reduces corn yield and contaminates infected kernels with the toxin fumonisin, which is harmful to humans and animals. Previous research has demonstrated that F. verticillioides can be controlled by the azole fungicide prochloraz. Currently, prochloraz is used as a foliar spray to control maize disease in China, which will increase the risk of resistance. Although F. verticillioides resistance to prochloraz has not been reported in the field, possible resistance risk and mechanisms resulting in prochloraz resistance were explored in the laboratory. Four prochloraz‐resistant strains of F. verticillioides were generated by successive selection on fungicide‐amended media. The mycelial growth rates of the mutants were inversely related to the level of resistance. All four mutants were cross‐resistant to the triazole fungicides triadimefon, tebuconazole and difenoconazole, but not to the multisite fungicide chlorothalonil or to the MAP /histidine‐kinase inhibitor fungicide fludioxonil. Based on the Y123H mutation in Fv CYP 51B, the four resistant mutants were subdivided into two genotypes: PCZ ‐R1 mutants with wildtype Fv CYP 51B and PCZ ‐R2 mutants with substitution Y123H in Fv CYP 51B. Wildtype Fv CYP 51B complemented the function of native Sc CYP 51 in Saccharomyces cerevisiae YUG 37:: erg11 , whereas Y123H‐mutated Fv CYP 51B did not. For the PCZ ‐R1 mutants, induced expression of Fv CYP 51A increased resistance to prochloraz. For the PCZ ‐R2 mutants, disruption of Fv CYP 51B function by the Y123H substitution caused constitutive up‐regulation of Fv CYP 51A expression and thus resistance to prochloraz.

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