Limited hypersensitive response but enhanced lignin synthesis leads to Pseudomonas syringae pv. actinidiae tolerance in Actinidia eriantha

Abstract Kiwifruit bacterial canker, caused by Pseudomonas syringae pv. actinidiae (Psa), poses a significant threat to the kiwifruit industry. Certain kiwifruit species, such as Eri-1 ( Actinidia eriantha ), exhibit resistance to Psa, as indicated by the minimal symptoms observed on their shoots and canes. However, discrepancies between leaf disease symptoms and resistance levels have been noted, and the underlying mechanisms remain poorly understood. This study explored the distinctive responses of Psa-resistant Eri-1 leaves to Psa infection. Upon inoculation, Eri-1 leaves activated protein kinase genes associated with pattern-triggered immunity (PTI), induced stomatal closure, and subsequently triggered resistance genes involved in effector-triggered immunity (ETI). However, suppression of downstream hypersensitive response (HR) signaling pathways in both PTI and ETI was observed, limiting reactive oxygen species (ROS) production and programmed cell death (PCD), thus impairing pathogen elimination. Additionally, upon Psa inoculation, the Psa-resistant Eri-1 predominantly activated lignin biosynthesis genes, while the Psa-susceptible ‘Hongyang’ activated flavonol biosynthesis genes within the shared phenylpropanoid pathway. This differential response mechanism facilitates Psa containment in Eri-1 leaves by promoting lignin accumulation, ultimately leading to pathogen elimination. These findings deepen our understanding of plant-pathogen interactions, providing insights into Psa pathogenesis and kiwifruit resistance, and offering valuable guidance for early-stage prevention and control strategies to mitigate crop losses.