Gummy stem blight (GSB), caused by Didymella bryoniae, is a devastating disease on watermelon. Pydiflumetofen belongs to succinate dehydrogenase inhibitor (SDHI) fungicide, which is effective in controlling many plant diseases. The EC50 values of 69 D. bryoniae isolates to pydiflumetofen ranged from 0.0018 to 0.0071 μg/mL, and the minimal inhibitory concentration (MIC) value of all strains to pydiflumetofen was <0.05 μg/mL. Eight pydiflumetofen-resistant mutants were obtained, and the level of resistance was stable. The mycelial growth, dry weight of mycelia, hyphal morphology, and pathogenicity of most resistant mutants did not change significantly compared with their parental strains, which indicated that the resistance risk of D. bryoniae to pydiflumetofen would be medium to high. Sequencing alignment showed that five resistant mutants presented a mutation at codon 277 (H277Y) in the SdhB gene. The point mutants FgSdhB H248Y/R exhibited decreased sensitivity to pydiflumetofen in Fusarium graminearum, which indicated that the point mutants of SdhB could reduce sensitivity to pydiflumetofen. These results further increase our understanding about the mode of action and the resistance mechanism of pydiflumetofen.

Fusarium fujikuroi, a causal agent of Rice Bakanae Disease, produces secondary metabolites such as gibberellin, pigments bikaverin, and mycotoxins fumonisins. Fumonisins produced by F. fujikuroi pose a severe threat to human and animal health. The copper chaperone protein plays a critical role in different growth stages of plants, fungi, and yeasts, but their functions and regulation in fumonisin biosynthesis are still unclear. Here, a copper chaperone protein, FfCOX17, was identified in F. fujikuroi. The FfCOX17 deletion mutant (∆FfCOX17) exhibited decreased vegetative growth and asexual reproduction. The transcriptional level of the FfFUM2 gene was significantly induced in ∆FfCOX17, and the fumonisin production in ∆FfCOX17 mutants was significantly increased compared to wild-type F. fujikuroi, but the pathogenicity of ∆FfCOX17 mutants was unaffected, which may be caused by the no significantly changed gibberellin content. ∆FfCOX17 showed decreased sensitivity to oxidative stress, osmotic stress, and increased sensitivity to cell wall stress, heat shock stress, and high concentration glucose. In addition, ∆FfCOX17 also showed increased sensitivity to fungicide fluazinam and fludioxonil, and decreased sensitivity to phenamacril and prochloraz. Taken together, this study suggested that FfCOX17 is critical for fumonisin production, vegetative growth, asexual reproduction, and fungicide sensitivity, but is not required for the virulence function of F. fujikuroi on rice.

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