The Role of FpfetC from Fusarium proliferatum in Iron Acquisition, Fumonisin B1 Production, and Virulence

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