Pseudomonas syringae Type III Effector Mediated Suppression of Innate Immunity in Arabidopsis and Soybean

Pathogens have evolved a multitude of effectors to subvert host immunity. The best studied examples are the type III effectors produced by Gram-negative bacterial pathogens, which are essential virulence proteins delivered directly into the host cytoplasm. Despite the identification of numerous type III effectors from plant and animal pathogens, the molecular basis of their functionalities in the hosts remains largely enigmatic. Particularly, very few direct targets of type III effectors have been identified. We use the Pseudomonas syringae Type III effector HopZ1 as a model to investigate the mechanisms underlying effector-mediated suppression of plant immunity. HopZ1 is a member of the widely distributed YopJ family of effectors produced by both plant and animal pathogens. Using the natural host soybean and the model organism Arabidopsis, we identified two direct virulence targets of HopZ1. In soybean, HopZ1 targets a key isoflavonoid biosynthetic enzyme, GmHID1, and inhibits the production of isoflavones. Isoflavones are precursors of phytoalexins, which have long been believed to play a role in antibiosis. In Arabidopsis, HopZ1 directly interacts with and induces the degradation of the Jasmonate-ZIM-domain (JAZ) proteins. JAZs are core negative regulators of the jasmonate (JA) signaling pathway, which is known to be antagonistic to the salicylic acid-mediated defense against biotrophic and hemibiotrphic pathogens. Overall, our data demonstrated that HopZ1 interferes with multiple pathways in plants to promote bacterial infection. This work discovered novel targets and strategies utilized by bacterial pathogens to cause diseases.