|LO, TIMOTHY - University Of Toronto|
|BASTEDO, PATRICK - University Of Toronto|
|GUTTMAN, DAVID - University Of Toronto|
|DESVEAUX, DARRELL - University Of Toronto|
Submitted to: Plant Signaling and Behavior
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/17/2013
Publication Date: 1/31/2014
Citation: Lewis, J.D., Lo, T., Bastedo, P., Guttman, D.S., Desveaux, D. 2014. The rise of the undead:Pseudokinases as mediators of effector-triggered immunity. Plant Signaling and Behavior. 9:e27563.
Interpretive Summary: Pseudomonas syringae is a bacterial pathogen that infects more than 100 plant species. P. syringae causes disease by injecting type III effector proteins into the plant. Recognition of specific type III effector proteins results in a rapid immune response that protects the plant from further infection. We identified an Arabidopsis thaliana pseudokinase ZED1 that is required for the recognition of the Pseudomonas syringe HopZ1a effector. We describe the role of kinases in the recognition of different effectors in the HopZ/YopJ/AvrRxv family. We present models of effector recognition in plants, and suggest that pseudokinases may act as decoys that trap effectors and allow immune recognition by the plant.
Technical Abstract: Pathogens use effector proteins to suppress host immunity and promote infection. However, plants can recognize specific effectors and mount an effector-triggered immune response that suppresses pathogen growth. The YopJ/HopZ family of type III secreted effector proteins is broadly distributed in bacterial pathogens of both animals and plants. These effectors can either suppress host immunity or elicit defense responses depending on the host genotype. In a recent report, we identified an Arabidopsis thaliana pseudokinase ZED1 that is required for the recognition of the Pseudomonas syringae HopZ1a effector. Here we discuss the role of ZED1 in HopZ1a recognition, and present models of effector recognition in plants. We draw parallels between HopZ1a and YopJ effector proteins, and between ZED1 and other immunity-related kinases that can be targeted by pathogen effectors.