Involvement of CYP51A, CYP51B, and CYP51C in the growth, reproduction, pathogenicity, and fungicide sensitivity of Fusarium oxysporum.

Fusarium oxysporum, a pathogenic fungus distributed worldwide, causes destructive diseases, such as plant wilt, crown rot, root rot, and fruit rot. Sterol demethylation inhibitors (DMIs), which are the most widely used fungicides, inhibit cytochrome P450 sterol 14α-demethylase (CYP51) during sterol biosynthesis. Fusarium species contain three homologous CYP51 genes, FoCYP51A, FoCYP51B, and FoCYP51C. Previous studies have shown that the deletion of individual CYP51 genes does not significantly affect phenotype-related indicators, such as growth rate and sporulation, in Fusarium species, such as F. graminearum, F. fujikuroi, and F. verticillioides. This study aimed to determine the effects of CYP51 genes on the growth, reproduction, pathogenicity, and DMI susceptibility of F. oxysporum. Unlike other Fusarium species, deletion of CYP51A reduced sporulation, germination, and pathogenicity, exacerbated cell membrane damage, and increased the DMI susceptibility in F. oxysporum. When a single CYP51 gene was knocked out, other CYP51 compensated by upregulating their expression to maintain balance. CYP51A could play a central role in this regulatory network. The absence of CYP51C did not cause noticeable changes in F. oxysporum. These results reveal the functional differentiation of FoCYP51 homologs in regulating growth, pathogenicity, and DMI susceptibility and provide an understanding of the pathogenic mechanisms and fungicide responses of F. oxysporum.