Abstract：
Pseudomonas syringae pv. actinidiae biovar 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 in Nicotiana benthamiana and is not recognised in susceptible A. chinensis cultivars. In a search for N. benthamiana nonhost resistance genes against HopZ5, we found that the nucleotide-binding leucine-rich repeat receptor NbPTR1 recognised HopZ5. RPM1-interacting protein 4 orthologues from N. benthamiana and A. chinensis formed a complex with NbPTR1 and HopZ5 activity was able to disrupt this interaction. No functional orthologues of NbPTR1 were found in A. chinensis. NbPTR1 transformed into Psa3-susceptible A. chinensis var. 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.
摘要：
丁香假单胞菌pv。猕猴桃biovar3（Psa3）在黄质猕猴桃（Actinidiachinensis）中引起毁灭性的溃疡病。效应HopZ5存在于所有Psa3分离株中，导致全球大流行猕猴桃溃疡病爆发，在烟草中触发免疫力，在易感的A.chinensis品种中不被识别。在寻找针对HopZ5的N.benthamiana非宿主抗性基因时，我们发现核苷酸结合的富含亮氨酸的重复序列受体NbPTR1识别HopZ5。来自N.benthamiana和A.chinensis的RPM1相互作用蛋白4直向同源物形成具有NbPTR1和HopZ5活性的复合物能够破坏这种相互作用。在A.chinensis中未发现NbPTR1的功能直系同源物。NbPTR1转化为Psa3易感的中国菜。中国Hort16A植物引入了对Psa3的HopZ5特异性抗性。总之,这项研究表明，在Psa3易感猕猴桃中表达NbPTR1是获得对Psa3抗性的可行方法，并且为在其他易感猕猴桃基因型中进行工程抗性提供了有价值的信息。
