A Novel Point Mutation (L837F) in Osmosensor-like Histidine Kinase FgOs1 Drives Potent Fludioxonil Resistance in Fusarium graminearum
Fusarium graminearum is a preeminent fungal pathogen exacting a heavy toll on global crop production. Fludioxonil, a highly effective broad-spectrum fungicide, has been extensively deployed to mitigate the devastation wrought by F. graminearum. Nevertheless, the molecular mechanisms of fludioxonil resistance in this pathogen remain largely enigmatic. In this study, we identify a novel point mutation (L837F) in FgOs1 (osmosensor-like histidine kinase), which is located in the HIS_KIN (histidine kinase) domain. Biological assays revealed that the FgOs1L837F mutation reduced the ability of F. graminearum to adapt to low-temperature stress, osmotic stress, and metal ion stress and also decreased its pathogenicity. Additionally, this mutation did not confer cross-resistance to the fungicides phenamacril, tebuconazole, and carbendazim. To facilitate field monitoring, we employed allele-specific PCR (AS-PCR) to detect FgOs1L837F point mutation in F. graminearum. This study offers crucial support for fungal disease control and crop protection.
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