Phenyllactic acid primed reactive oxygen species metabolism and phenylpropanoid pathway to induce resistance against Alternaria alternata in Malus domestica

Black spot rot, caused by the pathogen Alternaria alternata, is a prevalent disease in apple cultivation. The present study investigated the effects of phenyllactic acid (PLA) immersion on black spot rot in apples and elucidated the potential mechanisms underlying its action. Results revealed that 1.00 g L-1 PLA inhibited the lesion development in A. alternata- inoculated apples. PLA resulted in a decrease in malondialdehyde (MDA) content, while simultaneously increasing the levels of H2O2, ascorbic acid (AsA), and reduced glutathione (GSH) in apples. PLA also induced the increase in gene expressions and enzymatic activities of superoxide dismutase (SOD), catalase (CAT), monodehydroascorbate reductase (MDHAR), dehydroascorbic acid reductase (DHAR), ascorbate peroxidase (APX), glutathione reductase (GR), peroxidase (POD), polyphenol oxidase (PPO), cinnamate 4-hydroxylase (C4H), 4-coumarate/coenzyme A ligase (4CL), and phenylalanine ammonia lyase (PAL) in apples. Moreover, inoculation of both PLA-treated and control fruit with A. alternata led to a further increase in the levels of H2O2, GSH, and AsA, along with enhanced gene expressions and enzymatic activities of CAT, SOD, DHAR, GR, APX, MDHAR, POD, PPO, C4H, 4CL and PAL, compared to un-inoculated fruit. Additionally, PLA dipping increased total phenols and flavonoids contents in apples, and inoculation with A. alternata further augmented the accumulation of these bioactive compounds. Furthermore, PLA-treated fruit displayed a more rapid response to A. alternata inoculation compared to control fruit, characterized by heightened enzymatic activity, gene expression, and metabolite content. Collectively, PLA has the potential to stimulate disease resistance against A. alternata in apples through regulating major enzyme activities, gene expressions, and metabolites contents involved in reactive oxygen species and phenylpropane metabolisms.