Effector loss drives adaptation of Pseudomonas syringae pv. actinidiae biovar 3 to Actinidia arguta

A. arguta (kiwiberry) is resistant to Pseudomonas syringae pv. actinidiae biovar 3 (Psa3). This resistance is mediated via effector-triggered immunity as demonstrated by induction of the hypersensitive response. Isolates of Psa3 that cause lesions on A. arguta have been observed, however, and sequence analysis revealed a 49 kb deletion in the exchangeable effector locus (EEL). This natural EEL-mutant isolate and strains with synthetic knockouts of the EEL were more pathogenic on A. arguta plantlets than wild-type Psa3.

软枣猕猴桃（A. arguta, kiwiberry）对丁香假单胞菌猕猴桃致病变种生物型3（Pseudomonas syringae pv. actinidiae biovar 3，简称Psa3）具有抗性。该抗性通过效应子触发的免疫（effector-triggered immunity, ETI）介导，超敏反应的诱导即可证实该抗性通路。不过已有研究观测到能够在软枣猕猴桃上引发病斑的Psa3分离菌株，序列分析结果显示，此类菌株的可交换效应基因座（exchangeable effector locus, EEL）存在49 kb的片段缺失。相较于野生型Psa3，该天然EEL缺失突变株以及经人工基因敲除构建的EEL缺失菌株，对软枣猕猴桃组培苗的致病力显著更强。