Defence-related pathways, phytohormones and primary metabolism are key players in kiwifruit plant tolerance to Pseudomonas syringae pv. actinidiae

The reasons underlying the differential tolerance of Actinidia spp. to the pandemic pathogen Pseudomonas syringae pv. actinidiae (Psa) have not yet been elucidated. We hypothesized that differential plant-defence strategies linked to transcriptome regulation, phytohormones and primary metabolism might be key and that Actinidia chinensis susceptibility results from an inefficient activation of defensive mechanisms and metabolic impairments shortly following infection. Here, 48 h postinoculation bacterial density was 10-fold higher in A. chinensis var. deliciosa than in Actinidia arguta, accompanied by significant increases in glutamine, ornithine, jasmonic acid (JA) and salicylic acid (SA) (up to 3.2-fold). Actinidia arguta showed decreased abscisic acid (ABA) (0.7-fold), no changes in primary metabolites, and 20 defence-related genes that were only differentially expressed in this species. These include GLOX1, FOX1, SN2 and RBOHA, which may contribute to its higher tolerance. Results suggest that A. chinensis' higher susceptibility to Psa is due to an inefficient activation of plant defences, with the involvement of ABA, JA and SA, leading to impairments in primary metabolism, particularly the ammonia assimilation cycle. A schematic overview on the interaction between Psa and genotypes with distinct tolerance is provided, highlighting the key transcriptomic and metabolomic aspects contributing to the different plant phenotypes after infection.

Automated summary

Differential tolerance of Actinidia spp. to Pseudomonas syringae pv. actinidiae (Psa) may be linked to differential plant-defence strategies, phytohormones, and primary metabolism. Higher susceptibility of A. chinensis to Psa is attributed to inefficient activation of plant defences and metabolic impairments.