Roles of Paralogous CYP51 Genes in Biological Traits and Sensitivity to DMI Fungicides in Fusarium pseudograminearum

Fusarium crown rot, caused by Fusarium pseudograminearum, is a major wheat disease. Fungicide application is currently the main control method. Cytochrome P450 sterol 14α-demethylase (CYP51) is a key enzyme in the sterol biosynthesis pathway and the target of demethylation inhibitors (DMIs). This study investigated the roles of three FpCYP51 genes in fungal traits and DMI sensitivity. Deletion of FpCYP51A, FpCYP51B, or FpCYP51C did not affect conidiation, conidial germination, ergosterol biosynthesis, or trichothecene levels. However, mutants lacking FpCYP51B or both FpCYP51B and FpCYP51C exhibited reduced mycelial growth. Notably, ΔFpCYP51A and ΔFpCYP51AC mutants were more sensitive to ipconazole, mefentrifluconazole, metconazole, prochloraz, triadimefon, and tebuconazole. In contrast, ΔFpCYP51B and ΔFpCYP51BC mutants showed reduced DMI sensitivity, while ΔFpCYP51C had no effect on sensitivity. These results demonstrate that FpCYP51A and FpCYP51B are critical for regulating DMI sensitivity. The results provide important insights into the CYP51 function in plant pathogens and support the improved development of DMI fungicides.