Two plant NLR proteins confer strain-specific resistance conditioned by an effector from Pseudomonas syringaepv. actinidiae

Pseudomonas syringaepv. actinidiae(Psa) causes bacterial canker, a devastating disease threatening the Actinidiafruit industry. In a search for non-host resistance genes against Psa, we find that the nucleotide-binding leucine-rich repeat receptor (NLR) protein ZAR1 from both Arabidopsis and Nicotiana benthamiana(Nb) recognizes HopZ5 and triggers cell death. The recognition requires ZED1 in Arabidopsis and JIM2 in Nbplants, which are members of the ZRK pseudokinases and known components of the ZAR1 resistosome. Surprisingly, Arabidopsis ZAR1 and RPM1, another NLR known to recognize HopZ5, confer disease resistance to HopZ5 in a strain-specific manner. Thus, ZAR1, but not RPM1, is solely required for resistance to P. s. maculicolaES4326 (Psm) carrying hopZ5, whereas RPM1 is primarily required for resistance to P. s. tomatoDC3000 (Pst) carrying hopZ5. Furthermore, the ZAR1-mediated resistance to Psm hopZ5in Arabidopsis is insensitive to SOBER1, which encodes a deacetylase known to suppress the RPM1-mediated resistance to Pst hopZ5. In addition, hopZ5enhances P. syringaevirulence in the absence of ZAR1or RPM1 and that SOBER1abolishes such virulence function. Together the study suggests that ZAR1 may be used for improving Psaresistance in Actinidiaand uncovers previously unknown complexity of effector-triggered immunity and effector-triggered virulence.