Targeting the Snf1 kinase by cinnamaldehyde induces glucose starvation and oxidative stress in Fusarium solani for the control of sweet potato postharvest decay

Fusarium root rot, caused by Fusarium solani , is one of the major postharvest diseases of sweet potato. Cinnamaldehyde (CA), a natural product from cinnamon bark, has demonstrated promising antifungal efficacy; however, its mechanism of action, especially regarding fungal sugar metabolism, remains poorly understood. CA above 0.375 g L −1 inhibited F. solani mycelial growth, induced glucose deprivation, and triggered the accumulation of reserve carbohydrates (trehalose and glycogen). Moreover, CA promoted the accumulation of reactive oxygen species and hydrogen peroxide (H 2 O 2 ), protein carbonylation, and DNA fragmentation, indicating that CA caused oxidative damage and led to apoptotic cell death in F. solani . Notably, CA suppressed the function of the metabolic regulator sucrose non-fermenting protein kinase 1 (Snf1) by disrupting its transcription and translation. Genetic knockout of Snf1 increased the inhibition rate of mycelial growth, amplified intracellular glucose scarcity, promoted the accumulation of reserve carbohydrates, accelerated H 2 O 2 accumulation and protein oxidative damage, and ultimately exacerbated the extent of cell apoptosis. Complementarily, activation of Snf1 attenuated the antifungal effect of CA. Moreover, CA reduced rot incidence and better preserved nutritional quality (soluble sugars and starch), particularly in sweet potato roots infected with Snf1 -deletion mutants. These findings reveal that CA exerts its antifungal effect by disrupting Snf1-mediated glucose supply and inducing oxidative stress in F. solani to control sweet potato postharvest decay. This study provides novel insights into the antifungal mechanism of plant essential oils and supports the potential application of CA as an eco-friendly preservative for controlling postharvest spoilage in carbohydrate-rich fresh produce.