Fumonisin B1 induced aggressiveness and infection mechanism of Fusarium proliferatum on banana fruit.

Mycotoxins are increasingly considered as micropollutants in the environment. Fumonisins, as one of the most important mycotoxins, cause potential health threats to humans and animals due to their ubiquitous contamination on cereals, fruit, vegetables and other environmental samples around the world. However, the contribution of fumonisins to the interaction of fungi with plant hosts is not still fully understood. Here, we investigated the effect of fumonisin B1 (FB1) on the infection of Fusarium proliferatum on banana fruit and the underlying mechanisms from the host perspective. Our results found that FB1 treatment increased the aggressiveness of F. proliferatum on banana fruit and inhibited the defense ability of banana fruit via decreasing phenylalanine ammonia lyase (PAL), β-1,3-glucanase (GLU) and chitinase (CHI) activities. Meanwhile, FB1 accelerated cell death, indicated by higher relative conductivity, MDA content and higher transcripts of cell death-related genes. FB1 treatment resulted in higher hydrogen peroxide (H2O2) content possibly due to MaRBOHs induction. These consequences accelerated the ROS-dependent cell death, which subsequently result in reduction of disease resistance of banana fruit. Additionally, energy metabolism and MaDORN1s-mediated eATP signaling might involve in FB1-meidiated suppression of banana defense responses. Collectively, results of the current study indicated that FB1 contamination triggered the cell death of banana peel, subsequently instigating the invasion and growth of F. proliferatum on banana fruit. In summary, for the first time, we demonstrated a previously unidentified role of fumonisins as a potential virulence factor of F. proliferatum in modulating fruit defense response, which provides new insight on the biological roles of fumonisins.