Lipopeptide C₁₇ Fengycin B Exhibits a Novel Antifungal Mechanism by Triggering Metacaspase-Dependent Apoptosis in <i>Fusarium oxysporum</i>

Abstract

<i>Fusarium</i> wilt is a worldwide soil-borne fungal disease caused by <i>Fusarium oxysporum</i> that causes serious damage to agricultural products. Therefore, preventing and treating fusarium wilt is of great significance. In this study, we purified ten single lipopeptide fengycin components from <i>Bacillus subtilis</i> FAJT-4 and found that C₁₇ fengycin B inhibited the growth of <i>F. oxysporum</i> FJAT-31362. We observed early apoptosis hallmarks, including reactive oxygen species accumulation, mitochondrial dysfunction, and phosphatidylserine externalization in C₁₇ fengycin B-treated <i>F. oxysporum</i> cells. Further data showed that C₁₇ fengycin B induces cell apoptosis in a metacaspase-dependent manner. Importantly, we found that the expression of autophagy-related genes in the TOR signaling pathway was significantly upregulated; simultaneously, the accumulation of acidic autophagy vacuoles in <i>F. oxysporum</i> cell indicated that the autophagy pathway was activated during apoptosis induced by C₁₇ fengycin B. Therefore, this study provides new insights into the antifungal mechanism of fengycin.