Cinnamaldehyde triggers fungal apoptosis in Fusarium solani by impairing cell structures and antioxidant defense through restricting glucose availability

Fusarium solani is the primary causative agent of Fusarium root rot, one of major postharvest diseases of sweet potato. Cinnamaldehyde (CA) is a natural product isolated from cinnamon essential oil (EO). To combat the damage caused by F. solani, it is necessary to assess the antifungal activity of CA. The minimum inhibitory concentration (MIC) of CA against F. solani spores was 0.12 g/L, while addition of 2 % glucose increased the MIC to 0.16 g/L. A volatile concentration of CA at 0.12 g/L suppressed F. solani-induced root rot in sweet potatoes. Glucose addition alleviated CA-induced structural damage to cell walls and membranes. Moreover, CA reduced intracellular levels of glucose and glucose-6-phosphate (G6P), promoted oxidative stress, and induced cell apoptosis. However, glucose addition enhanced the gene expression of hexokinase and contents of glucose and G6P, thereby potentiating glycolytic flux. Further, sufficient glucose increased the gene expression of glutathione (GSH) reductase, GSH level, catalase activity, and decreased the contents of reactive oxygen species (ROS) and malondialdehyde in the presence of CA. Inhibition of glucose utilization using hexokinase inhibitor lonidamine (0.25 g/L) promoted ROS accumulation and exacerbated the reduction in cell viability of F. solani caused by 0.08 g/L CA. Altogether, these findings demonstrated that CA triggers fungal apoptosis by disrupting cell structures and antioxidant defense in F. solani mediated by glucose metabolism interference. Therefore, CA holds promise as a green preservative for sweet potato roots, and inhibition of glucose metabolism can serve as a novel strategy for enhancing the antifungal efficacy of EOs.