Defence-related pathways, phytohormones and primary metabolism are key players in the distinct tolerance of Actinidia spp. to pseudomonas syringae pv. actinidiae

The kiwifruit bacterial canker (KBC), caused by Pseudomonas syringae pv. actinidiae (Psa), affects plant yield and requires strict orchard management routines. Actinidia arguta (kiwi berry) is more tolerant than A. chinensis (green-fleshed kiwifruit) to Psa, but the molecular mechanisms that underpin plant tolerance are not fully understood. We hypothesised that plant tolerance is linked to the differential regulation of genes involved in distinct defence strategies shortly following infection. Here, micropropagated plants from both kiwifruit species were inoculated with Psa, and 48 hours post-inoculation, whole-transcriptome sequencing was performed. Psa density was 10-fold higher in A. chinensis than in A. arguta, demonstrating the tolerant character of the later species. Sixty-nine and 51 differentially expressed genes (DEGs) related with plant defences (e.g., pathogen recognition, immunity, and defence regulation) were identified in A. chinensis and A. arguta, respectively. Fifty-two DEGs related to abscisic (ABA), jasmonic (JA) and salicylic acid (SA) pathways, and 28 DEGs involved in primary metabolism (e.g., glycolysis, tricarboxylic acid and ammonia assimilation cycles) were also identified in A. chinensis, whereas in A. arguta 21 and 16 DEGs related with these biological functions, respectively, were identified. Results suggest that A. chinensis’ higher susceptibility to Psa is due to an inefficient activation of plant defence mechanisms, with the involvement of ABA, JA and SA, leading to impairments in primary metabolism. A. arguta’s increased tolerance may result from the downregulation of the ABA pathway and the expression of specific genes involved in plant defence, including FOX1, SN2 and RBOHA.