Kiwifruit has high economic value, but is susceptible to bacterial canker disease caused by Pseudomonas syringae pv. actinidiae (Psa). To dissect the resistance mechanisms, we performed an integrated transcriptomic and metabolomic analysis of a resistant species, Actinidia valvata , and a susceptible cultivar, A. chinensis ‘Hongyang’ (HY), following Psa infection. After Psa inoculation, a total of 1781 differentially expressed genes (DEGs) were identified collectively in HY and A. valvata , which were mainly annotated to 20 pathways, including plant-pathogen interaction, MAPK signaling pathway, and plant hormone signal transduction. Besides, 964 differentially accumulated metabolites (DAMs) were detected collectively in the two varieties, with 369 up-regulated and 595 down-regulated metabolites showing significant changes post-infection. Notably, flavonoids, phenolic acids, amino acids and alkaloids were the dominant DAMs, with A. valvata specifically accumulating key lignin-related metabolites (L-phenylalanine), while HY exhibited a net downregulation of most metabolites. DEGs and DAMs were co-enriched to 25 metabolic pathways, among which biosynthesis of various plant secondary metabolites was prominent. Key genes in the phenylpropanoid biosynthesis pathway were identified, genes related to lignin synthesis, including cinnamoyl-CoA reductase (CCR), cinnamyl alcohol dehydrogenase (CAD), and Peroxidase (POD), were significantly up-regulated in A. valvata , and their high expression levels correlated with reduced accumulation of lignin intermediates and elevated production of mature lignin polymers in A. valvata . This indicates that A. valvata likely contributes to enhanced lignin synthesis to defend against Psa infection, compared with HY. The results may elucidate the metabolic networks and molecular mechanisms of kiwifruit in response to bacterial canker disease.
Zhu et al. (Tue,) studied this question.