A sterol C-14 reductase encoded by FgERG24B is responsible for the intrinsic resistance of Fusarium graminearum to amine fungicides

Abstract

Fusarium graminearum, the causal agent of wheat head blight, shows intrinsic resistance to amine fungicides. It is commonly accepted that the amines target sterol C-14 reductase and sterol Δ8–Δ7isomerase of ergosterol biosynthesis, encoded by the genesERG24andERG2, respectively. Analysis of the genome sequence ofF. graminearumrevealed that the fungus contains two paralogousFgERG24genes (FgERG24AandFgERG24B), which are homologous to theERG24ofSaccharomyces cerevisiae. In this study, we disruptedFgERG24AandFgERG24BinF. graminearum. Compared to the wild-type strain HN9-1,FgERG24AandFgERG24Bdeletion mutants did not show recognizable phenotypic changes in mycelial growth on potato dextrose agar or in virulence on wheat heads. HPLC analysis showed that the amount of ergosterol inFgERG24AorFgERG24Bdeletion mutants was not significantly different from that in the wild-type strain. These results indicate that neither of the two genes is essential for growth, pathogenicity or ergosterol biosynthesis inF. graminearum.FgERG24Bdeletion mutants exhibited significantly increased sensitivity to amine fungicides, including tridemorph, fenpropidin and spiroxamine, but not to non-amine fungicides. In contrast,FgERG24Adeletion mutants did not show changed sensitivity to any amine tested. The resistance of theFgERG24Bdeletion mutant to amines was restored by genetic complementation of the mutant with wild-typeFgERG24B. These results indicate thatFgERG24Bcontrols the intrinsic resistance ofF. graminearumto amines. The finding of this study provides new insights into amine resistance in filamentous fungi.