The uncharacterized protein ZED2 contributes to immune activation in Arabidopsis following recognition of the Pseudomonas syringae effector HopZ1a
K. SCHREIBER (1), J. Hassan (2), M. Baudin (2), D. Nazarchuk (2), G. Walker (2), T. Helmann (2), J. Lewis (2) (1) University of California - Berkeley, U.S.A.; (2) University of California - Berkeley, U.S.A.

The recognition of pathogen virulence effector proteins by plant nucleotide-binding leucine-rich repeat (NLR) immune receptors elicits a localized cell death program termed the hypersensitive response (HR). While this response plays a critical role in plant disease resistance, the molecular components that facilitate effector-triggered immunity (ETI) remain to be fully characterized. Upon recognition of the Pseudomonas syringae effector HopZ1a, the Arabidopsis NLR HopZ-activated resistance 1 (ZAR1) stimulates an HR independently of known NLR signaling pathways. To identify additional host proteins involved in this response, we performed a forward genetic screen that yielded several Arabidopsis mutants with compromised HopZ1a-elicited immune responses. One of these mutants, named hopZ1a-ETI-deficient 2 (zed2), exhibited a delayed HR specifically in response to HopZ1a. This impaired response was corroborated by in planta growth assays which revealed that zed2 plants supported larger populations of P. syringae expressing HopZ1a than did wild-type plants. Pathogen-associated molecular pattern-triggered immunity was unaffected. Preliminary characterization of ZED2 by transient expression in Nicotiana benthamiana indicated that this protein is primarily nuclear-localized with some plasma membrane association. These data provide the first insights into the novel molecular mechanisms underlying HopZ1a-triggered immunity.

Abstract Number: P17-604
Session Type: Poster