Reduced Light Intensity Potentiates Resistance to Botrytis cinerea in Tomato by Directing Phenylpropanoid Flux Towards Lignification and Maintaining Reactive Oxygen Species Homeostasis

Botrytis cinerea is a devastating necrotrophic pathogen threatening global agriculture. Although modulating light intensity holds promise for sustainable disease management, the regulatory strategies and underlying mechanisms remain largely undefined. Three light intensity levels (200, 500 and 800 µmol·m −2 ·s −1 ) were applied in this study. By integrating multilevel pathological and cytological observations with transcriptional and metabolic pathway analyses, we systematically investigated how light intensity regulates defence responses against B. cinerea in tomato ( Solanum lycopersicum ). The results revealed that 200 µmol·m −2 ·s −1 light most effectively attenuated disease progression by orchestrating a multilayered defence network. This network encompasses stomatal closure to restrict pathogen invasion, phenylalanine‐derived lignin biosynthesis for cell wall reinforcement, upregulation of pathogenesis‐related proteins to facilitate pathogen degradation and maintenance of redox homeostasis to mitigate oxidative damage. These coordinated responses, rather than direct pathogen inhibition by light intensity, collectively restrict B. cinerea invasion. Application of exogenous phenylalanine and the PAL inhibitor 2‐aminoindan‐2‐phosphonic acid (AIP) further validated that light intensity dictates metabolic flux partitioning within the phenylpropanoid pathway, a core mechanism for enhanced resistance. This study provides the first evidence that low‐light‐induced resistance to B. cinerea stems from phenylpropanoid metabolic reprogramming and ROS homeostasis, offering novel insights into light‐modulated plant defence against necrotrophic pathogens.