Actigard™ induces a defence response to limit Pseudomonas syringae pv. actinidiae in Actinidia chinensis var. chinensis ‘Hort16A’ tissue culture plants.

Abstract

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. Actigard™, 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 Actigard™ 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. Actigard™ 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.