NbPTR1confers resistance againstPseudomonas syringae pv. actinidiaein kiwifruit

Abstract

AbstractPseudomonas syringae pv. actinidiaebiovar 3 (Psa3) causes a devastating canker disease in yellow-fleshed kiwifruit (Actinidia chinensis). The effector HopZ5, which is present in all isolates of Psa3 causing global outbreaks of pandemic kiwifruit canker disease, triggers immunity inNicotiana benthamianaand is not recognised in susceptibleA. chinensiscultivars. In a search forN. benthamiananon-host resistance genes against HopZ5, we found that the nucleotide-binding leucine-rich repeat receptor NbPTR1 recognised HopZ5. RPM1-interacting protein 4 (RIN4) orthologues from multiple plants, including kiwifruit, were associated with NbPTR1-mediated autoimmunity suppression and recognition of HopZ5. No functional orthologues of NbPTR1were found inA. chinensis. NbPTR1transformed into Psa3-susceptibleA. chinensisvar.chinensis‘Hort16A’ plants introduced HopZ5-specific resistance against Psa3. Altogether, this study suggested that expressing NbPTR1 in Psa3-susceptible kiwifruit is a viable approach to acquiring resistance to Psa3 and it provides valuable information for engineering resistance in otherwise susceptible kiwifruit genotypes.