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<p>Fusarium head blight (FHB), caused by <i>Fusarium graminearum</i>, is a globally significant fungal disease affecting wheat and barley crops. Chemical fungicides remain the primary control method. However, fungicide resistance remains a big challenge. This study assessed the sensitivity of field populations of <i>F. graminearum</i> from the Huang-Huai-Hai wheat region of China to the triazole fungicide propiconazole. All 101 isolates collected were sensitive, exhibiting EC<sub>50</sub> values ranging from 0.0210 to 0.4520&#xa0;µg/mL with a mean of 0.1740&#xa0;µg/mL. The unimodal frequency distribution of EC<sub>50</sub> values indicated no detectable resistance, establishing these values as a baseline sensitivity for monitoring regional <i>F. graminearum</i> populations. To evaluate the resistance risk, four propiconazole-resistant <i>F. graminearum</i> laboratory mutants were characterized. Stability testing across generations (1st, 3rd, 7th, and 10th) cultured without fungicide confirmed stable inheritance of the resistance phenotype. Evaluation of the biological fitness revealed significant (<i>p</i> &lt; 0.05) reductions in mycelial growth, sporulation, and pathogenicity in resistant mutants, although the spore germination rate increased. Molecular analysis of the CYP51 genes (<i>FgCYP51A</i>, <i>FgCYP51B</i>, and <i>FgCYP51C</i>), encoding sterol 14α-demethylase that target propiconazole, identified multiple point mutations conferring amino acid substitutions, including A101T, E102G, V104I, S168G, D247N, and G251R in FgCYP51A, V31A, and N272D in FgCYP51B and E164K, S256A, M273T, V307A, and V424E in FgCYP51C. Gene expression analysis showed consistent up-regulation of <i>FgCYP51A</i> and down-regulation of <i>FgCYP51B</i> and <i>FgCYP51C</i> in resistant mutants. Meanwhile, the study demonstrated cross-resistance between propiconazole and the demethylase inhibitor (DMI) fungicides prochloraz and difenoconazole. However, there is no cross-resistance between propiconazole and tebuconazole, difenoconazole, fluazinam, and carbendazim, this provides a basis for resistance management strategies such as rotating applications or mixing fungicides with different modes of action.</p>

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Sensitivity of Fusarium graminearum to propiconazole and potential resistance mechanisms

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年8月3日

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  • Feng Zhou,
  • Haichuan Su,
  • Jialin An,
  • Yan Jiao,
  • Zeyuan Chen,
  • Weiguo Li,
  • Haiyan Hu,
  • Chengwei Li,
  • Runqiang Liu

摘要

Fusarium head blight (FHB), caused by Fusarium graminearum, is a globally significant fungal disease affecting wheat and barley crops. Chemical fungicides remain the primary control method. However, fungicide resistance remains a big challenge. This study assessed the sensitivity of field populations of F. graminearum from the Huang-Huai-Hai wheat region of China to the triazole fungicide propiconazole. All 101 isolates collected were sensitive, exhibiting EC50 values ranging from 0.0210 to 0.4520 µg/mL with a mean of 0.1740 µg/mL. The unimodal frequency distribution of EC50 values indicated no detectable resistance, establishing these values as a baseline sensitivity for monitoring regional F. graminearum populations. To evaluate the resistance risk, four propiconazole-resistant F. graminearum laboratory mutants were characterized. Stability testing across generations (1st, 3rd, 7th, and 10th) cultured without fungicide confirmed stable inheritance of the resistance phenotype. Evaluation of the biological fitness revealed significant (p < 0.05) reductions in mycelial growth, sporulation, and pathogenicity in resistant mutants, although the spore germination rate increased. Molecular analysis of the CYP51 genes (FgCYP51A, FgCYP51B, and FgCYP51C), encoding sterol 14α-demethylase that target propiconazole, identified multiple point mutations conferring amino acid substitutions, including A101T, E102G, V104I, S168G, D247N, and G251R in FgCYP51A, V31A, and N272D in FgCYP51B and E164K, S256A, M273T, V307A, and V424E in FgCYP51C. Gene expression analysis showed consistent up-regulation of FgCYP51A and down-regulation of FgCYP51B and FgCYP51C in resistant mutants. Meanwhile, the study demonstrated cross-resistance between propiconazole and the demethylase inhibitor (DMI) fungicides prochloraz and difenoconazole. However, there is no cross-resistance between propiconazole and tebuconazole, difenoconazole, fluazinam, and carbendazim, this provides a basis for resistance management strategies such as rotating applications or mixing fungicides with different modes of action.