Nerol induces mitochondrial apoptosis and autophagy in Botrytis cinerea and its protection on postharvest cherry tomato.

Botrytis cinerea, the second prevalent fungal pathogen worldwide, threatens a wide range of plants through its aggressive gray mold infection. This study investigates the antifungal effect of nerol against B. cinerea. Its minimum inhibitory concentration is 0.25 mL/L. Colony diameter reduced by 88.86 % at 48 h. Nerol exposure induced ROS accumulation, increasing malondialdehyde levels, which disrupted membrane integrity. It further induced mitochondrial dysfunction by suppressing the enzyme activities of succinic dehydrogenase and citrate synthase, reducing membrane potential, and promoting cytochrome C release and caspase-3 activation. Combined with phosphatidylserine externalization, these results suggested that nerol inhibited the growth of B. cinerea by a mitochondrial apoptosis pathway. Nerol regulated autophagy-related genes expression and activated autophagy. In postharvest cherry tomatoes, nerol controlled gray mold on postharvest fruits by inhibiting the growth of B. cinerea, but also inducing fruit resistance by elevating phenolic content by 50.13 %. The study elucidates nerol's multifaceted antifungal and fruit-protective effects against B. cinerea, supporting its development for the postharvest preservation of cherry tomatoes.