HopF-triggered immunity in Arabidopsis requires a ZAR1/ZRK module
D. SETO (1), N. Koulena (2), T. Lo (2), D. Desveaux (2), D. Guttman (2) (1) University of Toronto, Canada; (2) University of Toronto, Canada

Pseudomonas syringae is a Gram-negative bacterial pathogen capable of infecting a wide range of plant species, including important crop species such as wheat, bean, and tomato. P. syringae possesses a needle-like type III secretion system, which is required for injecting effector proteins into plant cells. These effectors can disrupt the signaling components of the plant immune system, thereby promoting pathogen virulence. However, plants have evolved nucleotide-binding leucine rich repeat (NLR) proteins to recognize effectors and activate effector-triggered immunity (ETI) to counter pathogenesis. Effector recognition by NLR proteins can occur through direct interaction or indirectly, by monitoring for effector-induced modifications on specific host proteins. For example, the NLR protein ZAR1 indirectly recognizes the effectors HopZ1a and AvrAC by monitoring the host kinases that they target; ZED1 and PBL2, respectively. To avoid recognition by the plant immune system, P. syringae has diversified its collection of effectors to the point where ~60 families have been identified, each containing many allelic variants. The type III secreted effector HopF2 has previously been demonstrated to target kinases and promote P. syringae virulence in Arabidopsis. We present a novel HopF allele that elicits an ETI response in Arabidopsis. We show that this ETI response requires the ZAR1 NLR gene as well as a ZED-related kinase (ZRK). These results emphasize that the ZAR1 NLR protein has evolved to monitor multiple host kinases for effector-induced perturbations thereby broadening its recognition specificity and providing an effective guardian of the plant kinome. 

Abstract Number: P17-607
Session Type: Poster