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 nucleotidebinding le...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 nucleotidebinding leucine-rich repeat receptor(NLR)protein ZAR1 from both Arabidopsis and Nicotiana benthamiana(Nb)recognizes Hop Z5 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 resistosome.Surprisingly,Arabidopsis ZAR1 and RPM1,another NLR known to recognize Hop Z5,confer disease resistance to Hop Z5 in a strain-specific manner.Thus,ZAR1,but not RPM1,is solely required for resistance to P.s.maculicola ES4326(Psm)carrying hop Z5,whereas RPM1 is primarily required for resistance to P.s.tomato DC3000(Pst)carrying hop Z5.Furthermore,the ZAR1-mediated resistance to Psm hop Z5 in Arabidopsis is insensitive to SOBER1,which encodes a deacetylase known to suppress the RPM1-mediated resistance to Pst hop Z5.In addition,hop Z5 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 effectortriggered immunity and effector-triggered virulence.展开更多
基金supported by grants from the National Key R&D Program of China (2021YFA1300701) to J.M.Z.the National Natural Science Foundation of China (31872654) to Z.Y.Z.the Hainan Excellent Talent Team, and the State Key Laboratory of Plant Genomics (SKLPG2016B-2) to J.M.Z
文摘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 nucleotidebinding leucine-rich repeat receptor(NLR)protein ZAR1 from both Arabidopsis and Nicotiana benthamiana(Nb)recognizes Hop Z5 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 resistosome.Surprisingly,Arabidopsis ZAR1 and RPM1,another NLR known to recognize Hop Z5,confer disease resistance to Hop Z5 in a strain-specific manner.Thus,ZAR1,but not RPM1,is solely required for resistance to P.s.maculicola ES4326(Psm)carrying hop Z5,whereas RPM1 is primarily required for resistance to P.s.tomato DC3000(Pst)carrying hop Z5.Furthermore,the ZAR1-mediated resistance to Psm hop Z5 in Arabidopsis is insensitive to SOBER1,which encodes a deacetylase known to suppress the RPM1-mediated resistance to Pst hop Z5.In addition,hop Z5 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 effectortriggered immunity and effector-triggered virulence.
