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ARS Home » Pacific West Area » Albany, California » Plant Gene Expression Center » Research » Publications at this Location » Publication #299318

Research Project: Molecular Mechanisms of Plant Defense Signaling

Location: Plant Gene Expression Center

Title: The Arabidopsis ZED1 pseudokinase is required for ZAR1-mediated immunity induced by the Pseudomonas syringae type III effector HopZ1a

Author
item Lewis, Jennifer
item WAN, JANET - University Of Toronto
item HASSAN, JANA - University Of California
item LEE, AMY - University Of Toronto
item HURLEY, BRENDEN - University Of Toronto
item JHINGREE, JACQUELINE - University Of Toronto
item LO, TIMOTHY - University Of Toronto
item GUTTMAN, DAVID - University Of Toronto
item DESVEAUX, DARRELL - University Of Toronto

Submitted to: Proceedings of the National Academy of Sciences(PNAS)
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/8/2013
Publication Date: 10/29/2013
Citation: Lewis, J.D., Wan, J., Hassan, J.L., Lee, A.H., Hurley, B., Jhingree, J., Lo, T., Guttman, D.S., Desveaux, D. 2013. The Arabidopsis ZED1 pseudokinase is required for ZAR1-mediated immunity induced by the Pseudomonas syringae type III effector HopZ1a. Proceedings of the National Academy of Sciences. 110(46):18722-18727.

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 conducted a forward genetic screen to identify mutants that lack a rapid immune response to HopZ1a, P. syringae type III effector protein. We identified ZED1, a pseudokinase that is required specifically for the recognition of HopZ1a. In the absence of ZED1, Pseudomonas syringae carrying HopZ1a causes disease in the plant. We hypothesize that ZED1 alerts the host to the presence of the pathogen by acting as a trap for HopZ1a. This causes the induction of immune responses and protects the plant from pathogen infection.

Technical Abstract: Plant and animal pathogenic bacteria can suppress host immunity by injecting type III secreted effector (T3SE) proteins into host cells (1-5). However, T3SEs can also elicit host immunity if the host has evolved a means to recognize the presence or activity of specific T3SEs (6). The diverse YopJ/HopZ/AvrRxv T3SE superfamily, which is found in both animal and plant pathogens, provides examples of T3SEs playing this dual role (7). HopZ1a is an acetyltransferase carried by the phytopathogen Pseudomonas syringae that elicits Effector-Triggered Immunity (ETI) when recognized in Arabidopsis thaliana by the nucleotide-binding leucine-rich repeat (NB-LRR) protein ZAR1 (8-10). However, recognition of HopZ1a does not require any known ETI-related genes (10). Using a forward genetics approach we identify a novel ETI-associated gene that is essential for ZAR1-mediated immunity. The hopZ-ETI-deficient1 (zed1) mutant is specifically impaired in the recognition of HopZ1a, but not the recognition of other unrelated T3SEs or in PRR-triggered immunity. ZED1 directly interacts with both HopZ1a and ZAR1, and is acetylated on threonines 125 and 177 by HopZ1a. ZED1 is a non-functional kinase that forms part of small genomic cluster of kinases in Arabidopsis. We hypothesize that ZED1 acts as a decoy to lure HopZ1a to the ZAR1-resistance complex, resulting in ETI activation.