ActigardTM induces a defence response to limit Pseudomonas syringae pv. actinidiae in Actinidia chinensis var. chinensis 'Hort16A' tissue culture plants.

Bacterial canker, caused by the hemi-biotrophic pathogen Pseudomonas syringae pv. actinidiae (Psa), is the most serious disease of Actinidia species worldwide. Salicylic acid, a key plant defence hormone, plays a significant role in the induction of defence against Psa. ActigardTM, a salicylic acid mimic, is commonly used to manage Psa by priming the plants' endogenous salicylic acid-mediated defence response prior to infection. A considerable body of data exists on its effectiveness in orchard trials. Despite the horticultural significance, the dynamics of Psa populations in planta and the impact of ActigardTM priming on Psa survival overtime is difficult to follow given the numerous growth conditions and infection parameters that occur in the orchard environment. We set out to test whether a tissue culture system could be used to measure these properties. By correlating symptom development with endophytic Psa population growth, we demonstrate that disease development is controlled by a 'mechanistic switch', triggered by population size, which converts Psa from a biotrophic lifestyle to a necrotrophic lifestyle. ActigardTM treatment induced the expression of key salicylic acid defence genes to limit population growth resulting in an absence of disease-associated symptoms. Our data provides insight into the natural infection dynamics of Psa and the ability of the salicylic acid-mediated defence pathway to disrupt population growth and disease progression.

Automated summary

Bacterial canker, the most serious disease of kiwifruit caused by Pseudomonas syringae pv. actinidiae, is controlled by the key plant defense hormone salicylic acid and its mimic, ActigardTM. Research demonstrates that ActigardTM treatment induces expression of salicylic acid defense genes to limit pathogen growth and prevent disease symptoms.