Fumonisin B1 Biosynthesis Is Associated with Oxidative Stress and Plays an Important Role in <i>Fusarium proliferatum</i> Infection on Banana Fruit

Abstract

Fungal response to oxidative stress during infection on postharvest fruit is largely unknown. Here, we found that hydrogen peroxide (H₂O₂) treatment inhibited the growth of <i>Fusarium proliferatum</i> causing crown rot of banana fruit, confirmed by scanning electron microscopy (SEM) and transmission electron microscopy (TEM) observation. H₂O₂ exposure increased endogenous reactive oxygen species (ROS) and fumonisin B1 (FB1) production in <i>F. proliferatum</i>, possibly by modulating <i>FUM</i> or ROS-related gene expression. Importantly, H₂O₂ treatment inhibited <i>F. proliferatum</i> growth <i>in vivo</i> but induced FB1 accumulation in banana peel. Finally, we constructed the <i>FpFUM</i>21 deletion mutant (Δ<i>Fpfum</i>21) of <i>F. proliferatum</i> that was attenuated in FB1 biosynthesis and less tolerant to oxidative stress. Moreover, the Δ<i>Fpfum</i>21 strain was less virulent compared to the wild type (WT) due to the inability to induce FB1 production in the banana host. These results suggested that FB1 biosynthesis is associated with oxidative stress in <i>F. proliferatum</i> and contributes to fungal infection on banana fruit.