Fusarium graminearum species complex (FGSC), causing Fusarium head blight (FHB) of wheat, has species-specific geographical distributions in wheat-growing regions. In recent years, benzimidazole resistance of FHB pathogens has been largely widespread in China. Although the demethylation inhibitor fungicide metconazole has been used for FHB control in some countries, no information about metconazole sensitivity of Chinese FHB pathogen populations and efficacy of metconazole in FHB control in China is available. In this study, the sensitivity of FGSC to metconazole was measured with 32 carbendazim-sensitive strains and 35 carbendazim-resistant strains based on mycelial growth. The 50% effective concentration values of 67 strains were normally distributed and ranged from 0.0209 to 0.0838 μg ml−1, with a mean of 0.0481 ± 0.0134 μg ml−1. No significant difference in metconazole sensitivity was observed between carbendazim-sensitive and -resistant populations. An interactive effect of metconazole and phenamacril, a novel cyanoacrilate fungicide approved in China against Fusarium spp., in inhibiting mycelial growth showed an additive interaction at different ratios. Furthermore, field trials to evaluate the effect of metconazole and metconazole + phenamacril treatments in FHB control, deoxynivalenol (DON) production, and grain yields were performed. Compared with the fungicides carbendazim and phenamacril currently used in China, metconazole exhibits a better efficacy for FHB control, DON production, and grain yields, and dramatically reduces use dosages of chemical compounds in the field. The mixture of metconazole and phenamacril at ratios of 2:3 and 1:2 showed the greatest efficacy for FHB control, DON production, and grain yields among all the fungicide treatments but its use dosages were higher in comparison with metconazole alone. In addition, FHB control, grain yields, and DON levels were significantly correlated with each other, showing that visual disease indices can be used as an indicator of grain yields and DON contamination. Meanwhile, the frequency of carbendazim-resistant alleles in F. graminearum populations was dramatically reduced after metconazole and phenamacril alone and the mixture of metconazole and phenamacril applications, indicating that metconazole and a mixture of metconazole and phenamacril can be used for carbendazim resistance management of FHB in wheat. Overall, the findings of this study provide important data for resistance management of FHB and reducing DON contamination in wheat grains.

Deoxynivalenol (DON) is a vital virulence factor of Fusarium graminearum, which causes Fusarium head blight (FHB). We recently found that validamycin A (VMA), an aminoglycoside antibiotic, can be used to control FHB and inhibit DON contamination, but its molecular mechanism is still unclear. In this study, we found that both neutral and acid trehalase (FgNTH and FgATH) are the targets of VMA in F. graminearum, and the deficiency of FgNTH and FgATH reduces the sensitivity to VMA by 2.12‐ and 1.79‐fold, respectively, indicating that FgNTH is the main target of VMA. We found FgNTH is responsible for vegetative growth, FgATH is critical to sexual reproduction, and both of them play an important role in conidiation and virulence in F. graminearum. We found that FgNTH resided in the cytoplasm, affected the localization of FgATH, and positively regulated DON biosynthesis; however, FgATH resided in vacuole and negatively regulated DON biosynthesis. FgNTH interacted with FgPK (pyruvate kinase), a key enzyme in glycolysis, and the interaction was reduced by VMA; the deficiency of FgNTH affected the localization of FgPK under DON induction condition. Strains with a deficiency of FgNTH were more sensitive to demethylation inhibitor (DMI) fungicides. FgNTH regulated the expression level of FgCYP51A and FgCYP51B by interacting with FgCYP51B. Taken together, VMA inhibits DON biosynthesis by targeting FgNTH and reducing the interaction between FgNTH and FgPK, and synergizes with DMI fungicides against F. graminearum by decreasing FgCYP51A and FgCYP51B expression.

Fusarium head blight (FHB), caused by the Fusarium graminearum species complex, is a devastating fungal disease resulting in substantial yield and quality losses. Ergosterol biosynthesis inhibitors (EBIs) are the most popular chemicals for controlling FHB. Recently, the resistance of F. graminearum to EBIs has emerged in the field, and an amino acid substitution (G443S) of the sterol 14α-demethylase FgCYP51A was detected in the field resistant strains. To further illustrate the resistance mechanism of F. graminearum to EBIs, site-directed mutants conferring the G443S substitution of FgCYP51A were generated from the progenitor strain PH-1 via genetic transformation with site-directed mutagenesis. We found that the FgCYP51A-G443S substitution significantly decreased the sensitivity of F. graminearum to EBIs with EC 50 values ranging from 0.1190 to 0.2302 μg mL −1 and EC 90 values ranging from 1.3420 to 9.1119 μg mL −1 for tebuconazole. Furthermore, the FgCYP51A-G443S substitution decreased sexual reproduction and virulence, which will reduce the initial infection source of pathogen populations in the field, while the increase of sporulation capability may enhance the frequencies of the disease cycle, thereby contributing to epidemics of FHB disease. Surprisingly, the FgCYP51A-G443S substitution accelerated DON biosynthesis by upregulating TRI5 expression and enhancing the fluorescence intensity of TRI1-GFP, the marker protein of Fusarium toxisomes. Thus, we concluded that the FgCYP51A-G443S substitution regulates EBI-fungicide resistance and DON biosynthesis, increasing the risk of fungicide resistance development in the field, thereby threatening the control efficacy of EBIs against FHB.

Sclerotinia sclerotiorum is a devastating plant pathogen with a broad host range and worldwide distribution. The application of chemical fungicides is a primary strategy for controlling this pathogen. However, under the high selective pressure of chemical fungicides, fungicide resistance has emerged and gradually increased, resulting in the failure to control S. sclerotiorum in the field. Quinofumelin is a novel quinoline fungicide, but its antifungal activities against plant pathogens have been rarely reported. Here, we determined the antifungal activity of quinofumelin against S. sclerotiorum in vitro and in planta. The EC50 values ranged from 0.0004 to 0.0059 μg mL-1 with a mean EC50 of 0.0017 ± 0.0009 μg mL-1 and were normally distributed (P=0.402). In addition, no cross-resistance was observed between quinofumelin and other fungicides, dimethachlone, boscalid, or carbendazim, which are commonly used to manage S. sclerotiorum. Quinofumelin did not affect glycerol and oxalic acid production of either carbendazim-sensitive or -resistant isolates. Moreover, quinofumelin exhibited excellent protective, curative, and translaminar activity against S. sclerotiorum on oilseed rape leaves. Protective activity was higher than curative activity. Interestingly, quinofumelin inhibited the formation of the infection cushion in S. sclerotiorum, which may contribute to the control efficacy of quinofumelin against S. sclerotiorum in the field. Our findings indicate that quinofumelin has excellent control efficacy against S. sclerotiorum in vitro and in planta as compared with the currently extensively used fungicides and could be used to manage carbendazim- and dimethachlone-resistance in S. sclerotiorum in the field.

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