Pathogenicity and Virulence‐Associated Factors of <i>Pseudomonas syringae</i> pv. <i>syringae</i> and [ <i>P. amygdali</i> pv. <i>morsprunorum</i> ] Strains From New Zealand Sweet Cherry ( <i>Prunus avium</i> ) Orchards

ABSTRACT Previously genetically characterised strains of Pseudomonas syringae. pv. syringae (Pss), [ P. amygdali pv. morsprunorum ] (Pam, syn. P. s . pv. morsprunorum race 1) and Pseudomonas spp. from New Zealand were characterised for their pathogenicity and aggressiveness in plant tissue and associated virulence factors. Lesions on detached, Pss‐inoculated immature fruit increased rapidly in size and, at 10 days post inoculation (dpi), had larger areas under the disease progress curve (AUDPC) than Pam‐inoculated fruit (48.9 and 22.0, respectively). Detached leaves infiltrated with Pss‐developed symptoms within 1 dpi and from 2 dpi for Pam. Necrosis from most Pss strains extended into the leaf veins by 7 dpi, while Pam strains' necrosis was confined to the inoculation site. On detached 1‐year‐old cherry shoots, Pseudomonas spp. strains exhibited the smallest mean lesion size (2.1–2.4 mm), whereas larger mean lesion sizes were observed with Pss strains (5.7–13.7 mm) and Pam strains (3.9–14.0 mm). A functional T3SS was inferred for Pss and Pam strains based on the hypersensitivity reactions observed on tobacco leaves and symptoms elicited on cherry tissue. Syringomycin production was prevalent (88%) among Pss strains. In contrast, only 1.4% of Pam strains produced coronatine. Most Pss strains (97.0%) were able to catalyse ice formation. The coexistence of strains with varying degrees of virulence and non‐pathogenic strains suggests a complex ecological balance, where multiple factors, including genetic variation, virulence traits and environmental conditions, shape the population dynamics and disease outcomes.