Kiwifruit Bacterial Canker Susceptibility of 86 Accessions and Their Physiological Response to Psa Inoculation

Abstract

Kiwifruit bacterial canker, caused by Pseudomonas syringae pv. actinidiae (Psa), severely restricts the sustainable development of the kiwifruit industry. Screening stable resistant germplasm and establishing efficient disease resistance evaluation methods are core prerequisites for breeding resistant cultivars. In this study, 86 Actinidia accessions were systematically assessed for Psa susceptibility over three consecutive years using the reported detached shoot inoculation assay. Seven representative accessions with contrasting resistance phenotypes, namely ‘Cuiyu’, ‘Chuhong’, ‘Jinmei’, ‘Hongyang’, ‘Cuixiang’, ‘Avfs08’, and ‘G3’, were selected to measure the activities of four defense-related enzymes post Psa inoculation to dissect the physiological mechanisms driving divergent Psa resistance in kiwifruit. Lesion lengths across years exhibited a significant positive correlation, demonstrating that this inoculation method delivers repeatable, genetically stable phenotypic data with limited environmental interference. Two accessions belonging to A. valvata and A. eriantha exhibited stable high resistance via synergistic biochemical defenses. By contrast, the widely grown cultivar ‘Hongyang’ was highly susceptible, while moderately resistant materials such as ‘Cuiyu’ and ‘Yannong 3’ were discovered within the inherently susceptible species A. chinensis. Highly resistant accessions rapidly induced coordinated increases in SOD and PAL activity at 24 h post inoculation to maintain ROS homeostasis and lignin biosynthesis, whereas susceptible accessions displayed chaotic, ineffective enzymatic stress responses. Temporal synergy of PAL and POD may act as the key defensive regulatory mode. This study uncovered substantial interspecific variation in Psa resistance across Actinidia germplasm, identified elite donors with stable resistance, and elucidated the physiological mechanisms of kiwifruit resistance to Psa. These findings provided a theoretical foundation and valuable germplasm for subsequent resistance gene mining and disease resistance breeding.