摘要Pseudomonas syringae pv.actinidiae(Psa)causes bacterial canker,a devastating disease threatening the Actinidia fruit 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 Nb plants,which are members of the ZRK pseudokinases and known components of the ZAR1 resisto-some.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.maculicola ES4326(Psm)carrying hopZ5,whereas RPM1 is primarily required for resistance to P.s.tomato DC3000(Pst)carrying hopZ5.Furthermore,the ZAR1-mediated resistance to Psm hopZ5 in Ara-bidopsis is insensitive to SOBER1,which encodes a deacetylase known to suppress the RPM 7-mediated resistance to Pst hopZ5.In addition,hopZ5 enhances P.syringae virulence in the absence of ZAR1 or RPM1 and that SOBER1 abolishes such virulence function.Together the study suggests that ZAR1 may be used for improving Psa resistance in Actinidia and uncovers previously unknown complexity of effector-triggered immunity and effector-triggered virulence.