Arachidonic acid enhances gray mold resistance in postharvest tomato via modulating phenylpropanoid biosynthesis, plant-pathogen interaction, and MAPK signaling pathway

Cherry tomatoes (Solanum lycopersicum var. cerasiforme), an economically important crop, are highly susceptible to gray mold caused by Botrytis cinerea during postharvest storage, resulting in deterioration of fruit quality. As a polyunsaturated fatty acid, arachidonic acid (ARA) has been shown to act as an elicitor to induce plant defense responses against pathogens. In the present work, we explored the inducing effects and mechanisms of ARA on gray mold resistance through physiological and transcriptomic analyses. Exogenous ARA increased the activities of defense-related enzymes, such as polyphenol oxidase, peroxidase, catalase, phenylalanine ammonia-lyase, and ascorbate peroxidase, as well as significantly suppressed malondialdehyde accumulation in tomato. Transcriptomic analyses revealed that ARA treatment highlighted coordinated changes in the key pathways, including phenylpropanoid biosynthesis, plant-pathogen interaction, and MAPK signaling pathway, resulting in enhanced resistance against B. cinerea in tomato. The up-regulation of calcium signaling-related genes (CDPK and CNGCs) induced early reactive oxygen species burst and hypersensitive response. MEKK1-MKK1/2-MPK4 and MEKK1-MKK4/5-MPK3/6 cascade in the MAPK signaling pathway regulated transcription factors (WRKY25/33, WRKY22/29, Pti5, and Pti6), which in turn induced defense-related genes (PR1 and ChiB). Concurrently, the upregulation of key genes (4CL, PAL, POD, CCoAOMT, and CYP98A3) in the phenylpropanoid metabolic pathway promoted lignin deposition and the accumulation of antimicrobial compounds, establishing a dual-layered physical-chemical defense barrier. This study provides new insights into the resistance of cherry tomato against B. cinerea induced by ARA.