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BACKGROUND: Wheat Fusarium crown rot (FCR) is a serious problem primarily caused by Fusarium pseudograminearum, a pathogenic agent known to produce mycotoxins, including deoxynivalenol (DON). Cyclobutrifluram, a novel succinate dehydrogenase inhibitor devised by Syngenta, has immense potential to control both nematodes and Fusarium diseases. However, its efficacy in combating Fusarium species, its ability to prevent and reverse the detrimental effects of FCR, and its impact on the production of DON by F. pseudograminearum are yet to be fully ascertained. RESULTS: Cyclobutrifluram exhibited substantial inhibitory activity against Fusarium species, with half‐maximal effective concentration values ranging from 0.0021–0.0647 μg mL−1. It demonstrated significant inhibitory activity toward three developmental stages of F. pseudograminearum, F. graminearum and F. asiaticum. Furthermore, cyclobutrifluram showed both protective and curative activities against FCR and was rapidly absorbed by roots and transported to wheat stems and leaves. Cyclobutrifluram could also decrease DON production by F. pseudograminearum. CONCLUSION: This investigation has revealed the potential of cyclobutrifluram as a formidable candidate fungicide, particularly in its ability to effectively combat FCR and other Fusarium‐related ailments. This novel compound has exceptional pathogen‐fighting capabilities, coupled with remarkable systemic translocation properties and a notable ability to reduce the production of DON. © 2023 Society of Chemical Industry. [ABSTRACT FROM AUTHOR]

Cyclobutrifluram is a novel succinate dehydrogenase inhibitor (SDHI) developed by Syngenta and helps to inhibit Fusarium pseudograminearum . Here, the potential for cyclobutrifluram resistance in F. pseudograminearum and the resistance mechanism involved were evaluated. Baseline sensitivity of F. pseudograminearum to cyclobutrifluram was determined with a mean EC 50 value of 0.0248 μg/mL. Fungicide adaption generated five resistant mutants, which possess a comparable or a slightly impaired fitness compared to corresponding parental isolates. This indicates that the resistance risk of F. pseudograminearum to cyclobutrifluram might be moderate. Cyclobutrifluram-resistant isolates also demonstrated resistance to pydiflumetofen but sensitivity to carbendazim, phenamacril, tebuconazole, fludioxonil, or pyraclostrobin. Additionally, point mutations H248Y in FpSdhB and A83V or R86K in FpSdhC 1 were found in cyclobutrifluram-resistant F. pseudograminearum mutants. Molecular docking and overexpression transformation assay revealed that FpSdhB H248Y and FpSdhC 1 A83V or FpSdhC 1 R86K confer the resistance of F. pseudograminearum to cyclobutrifluram.