Abstract
Diaporthe eres is a harmful pathogen affecting Hongyang kiwifruit (Actinidia chinensis) after harvest, yet the antioxidant defense strategies are not well understood. This research thoroughly examines the dynamics of the antioxidant response during the infection process. Significant findings indicate an initial 3-day latent period (0-3 dpi) that allowed for pathogen establishment, followed by irreversible tissue breakdown characterized by water-soaked lesions at 4 dpi. The study identified a biphasic activation pattern of superoxide dismutase (SOD) with dual activity peaks (1 dpi and 4 dpi), orchestrated by mitochondrial hub gene CEY00_Acc02790 that coordinates peroxidase (POD) networks, while peroxidase (POD) activity exhibited a synchronized but temporary increase, peaking at 4 dpi. Further bioinformatic analysis revealed the possible functional specialization of POD isoforms: α-helix-rich extracellular variants drove cell wall reinforcement through lignification, while random coil-dominant intracellular variants formed to mitigate cytoplasmic reactive oxygen species (ROS) damage, establishing dual physicochemical barriers. Malondialdehyde (MDA) levels rose significantly by 3 dpi, indicating permanent membrane damage. Collectively, these findings elucidate the mechanistic foundation of the Actinidia-Diaporthe pathosystem, identifying the bimodal SOD response and POD specialization as prime targets for developing resistant cultivars and precision postharvest interventions, ultimately reducing losses through biochemical interception of pathogenesis.