Type III effector repertoires as a window into Pseudomonas syringae pv. actinidiae evolution and Actinidia defense...

Kiwifruit bacterial canker, caused by Pseudomonas syringae pv. actinidiae (Psa), represents a complex disease system in which closely related bacterial populations differ in host association, pathogenicity, genomic composition, and geographic distribution as evidenced by pandemic spread of biovar 3 after 2008. Closely related Psa lineages differ in host association, virulence, and distribution, yet these differences arise largely outside the conserved core genome. Mobile genetic elements remodel accessory regions, and acquisition, loss, and redundancy of type III effectors shape whether a lineage colonizes or is restricted by a given Actinidia genotype. Virulence is therefore a host-dependent property, not a fixed lineage rank. On the host side, genome assemblies, QTL mapping, and infection transcriptomics indicate that resistance reflects the timing and persistence of immune signalling rather than receptor presence alone, although few candidate receptors have been validated in planta. Durable resistance is most likely to derive from recognition of non-redundant effector functions and from immune hubs, such as RIN4, that multiple effectors target. Integrating pathogen population genomics, effector biology, and host immune genetics is the route to predicting which lineages will emerge next.