Fusarium asiaticum is a critical pathogen of Fusarium head blight (FHB) in the southern part of China. The fungicide phenamacril has been extensively used for controlling FHB in recent years, which reduced both FHB severity and mycotoxin production. Our previous report indicated that resistance of F. asiaticum to phenamacril was related to mutations in myosin5. A recent article revealed that the resistance level of phenamacril-resistant mutants was associated with the genotypes of myosinS in these mutants. In total, we obtained 239 resistant isolates by fungicide domestication, and 82 resistant mutants were randomly selected for further study. Of these mutants, 25.6,7.3, and 67.1 % showed low resistance (LR), moderate resistance (MR), and high resistance (HR), respectively, to phenamacril determinedby 50% effective concentration values. Point mutations A135T, V151M. P204S, I434M, A577T, R580G/H, or 158IF led to LR. Point mutations S418R, I424R, and A577G were responsible for MR and point mutations K216R/E, S217P/L, or E420K/G/D conferred HR. Interestingly, all of the mutations concentrated in the myosin5 motor domain and mutations conferring HR occurred at codon 217 and 420, which we called the core region. Homology modeling revealed that mutations far from the core region led to a lower resistance degree. Phenotype assays revealed that the most highly resistant mutants did not significantly change pathogenicity but decreased conidia production compared with the wild type, which may slow down the formation of the resistant pathogen population inthe fields.
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