Risk and Molecular Mechanism of Metconazole Resistance in the Rice Bakanae Pathogen Fusarium fujikuroi
TL;DR
The resistance risk of F. fujikuroi to metconazole is assessed as low, and the binding between metconazole and FfCYP51B-G464S was weakened, and the binding free energy was less favorable.
Abstract
Rice bakanae disease, caused by Fusarium fujikuroi, is a destructive seed-borne disease. Metconazole has excellent control potential, but its resistance risk and mechanism remain unreported. This study confirmed metconazole has strong antifungal activity, with EC50 values ranging from 0.0073 to 0.0468 μg/mL. After fungicide taming, we obtained seven metconazole-resistant mutants with low-level, genetically stable resistance. Biological fitness showed mycelial growth and virulence did not decrease significantly, but sporulation increased significantly. Cross-resistance found the mutants had cross-resistance to tebuconazole, prochloraz, triticonazole and difenoconazole, but not to prothioconazole, prothioconazole-desthio, epoxiconazole, ipconazole, propiconazole, triadimefon, fludioxonil, or pyraclostrobin. Sequence analysis detected the G464S substitution in FfCYP51B in all mutants, which site-directed mutagenesis confirmed reduces metconazole sensitivity. Molecular docking, dynamics simulation and MM/GBSA analysis showed the binding between metconazole and FfCYP51B-G464S was weakened, and the binding free energy was less favorable. In conclusion, the resistance risk of F. fujikuroi to metconazole is assessed as low.