Abstract：
Fusarium wilt is a worldwide soil-borne fungal disease caused by Fusarium oxysporum 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 Bacillus subtilis FAJT-4 and found that C17 fengycin B inhibited the growth of F. oxysporum FJAT-31362. We observed early apoptosis hallmarks, including reactive oxygen species accumulation, mitochondrial dysfunction, and phosphatidylserine externalization in C17 fengycin B-treated F. oxysporum 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 F. oxysporum 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.
摘要：
枯萎病是由尖孢镰刀菌引起的世界性土传真菌病，对农产品造成严重危害。因此,防治枯萎病具有重要意义。在这项研究中,我们从枯草芽孢杆菌FAJT-4中纯化了10个单一的脂肽fengycin成分，发现C17fengycinB抑制了尖孢芽孢杆菌FJAT-31362的生长。我们观察到早期细胞凋亡的标志，包括活性氧的积累，线粒体功能障碍，和磷脂酰丝氨酸外化在C17风霉素B处理的尖孢酵母细胞中。进一步的数据显示，C17芬霉素B以超半胱氨酸蛋白酶依赖性方式诱导细胞凋亡。重要的是,我们发现自噬相关基因在TOR信号通路中的表达显著上调;同时,酸性自噬空泡在尖孢酵母细胞中的积累表明自噬途径在C17风霉素B诱导的细胞凋亡过程中被激活。这项研究为芬霉素的抗真菌作用机制提供了新的见解。
