Abstract
Iron is an essential micronutrient required for the fungal growth and propagation. Fusarium proliferatum is the causal agent of rice spikelet rot disease. In this study, we characterized the role of F. proliferatum multicopper ferroxidase (FpfetC), which mediated the oxidization of ferrous to ferric iron in the reductive system of iron assimilation. Deletion of FpfetC led to impaired growth under iron-deprived conditions, and the growth defect could be restored by exogenous iron. Compared to wild-type Fp9 strain, ΔFpfetC showed increased conidiation, resistance to copper stress, and sensitivity to zinc stress. FpfetC deficiency rendered a transcription remodeling of genes involved in high-affinity iron assimilation, iron homeostasis and iron storage. Moreover, production of fumonisin B1 (FB1) and transcript levels of fumonisin biosynthesis (Fpfums) genes were elevated in ΔFpfetC. ΔFpfetC exhibited hypervirulence to rice, accompanied with aggravation of invasive hyphae and activation of siderophore synthesis at the sites of inoculation. Additionally, disruption of FpfetC attenuated penetration ability to cellophane membrane under iron starvation. Taken together, these results demonstrated that FpfetC played important roles in iron uptake, conidiation, response to metal stress, fumonisin biosynthesis, and virulence in F. proliferatum.