State Key Laboratory of Plant Genomics, Institute of Genetics and Developmental Biology, The Innovative Academy of Seed Design, Chinese Academy of Sciences, Beijing 100101, China; CAS Center for Excellence in Biotic Interactions, University of Chinese Academy of Sciences, Beijing 100049, China.
College of Horticulture, China Agricultural University, Beijing 100193, China.
J Genet Genomics. 2022 Aug;49(8):823-832. doi: 10.1016/j.jgg.2022.06.006. Epub 2022 Jun 24.
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 resistosome. 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 Arabidopsis is insensitive to SOBER1, which encodes a deacetylase known to suppress the RPM1-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.
丁香假单胞菌 pv. 猕猴桃溃疡病（Psa）引起细菌性溃疡病，是一种严重威胁猕猴桃产业的毁灭性疾病。在寻找非寄主抗性基因以对抗 Psa 的过程中，我们发现拟南芥和烟草（Nb）中的核苷酸结合亮氨酸重复受体（NLR）蛋白 ZAR1 识别 HopZ5 并引发细胞死亡。这种识别需要拟南芥中的 ZED1 和 Nb 植物中的 JIM2，它们是 ZRK 类蛋白激酶的成员，也是 ZAR1 抗病体的已知组成部分。令人惊讶的是，拟南芥 ZAR1 和 RPM1，另一种已知识别 HopZ5 的 NLR，以菌株特异性方式赋予对 HopZ5 的抗病性。因此，ZAR1，但不是 RPM1，是唯一需要抵抗携带 hopZ5 的 P. s. maculicola ES4326（Psm）的，而 RPM1 主要需要抵抗携带 hopZ5 的 P. s. tomato DC3000（Pst）。此外，ZAR1 介导的对拟南芥中 Psm hopZ5 的抗性对 SOBER1 不敏感，SOBER1 编码一种已知抑制 RPM1 介导的对 Pst hopZ5 的抗性的脱乙酰酶。此外，在缺乏 ZAR1 或 RPM1 的情况下，hopZ5 增强了丁香假单胞菌的毒力，而 SOBER1 则消除了这种毒力功能。综上所述，该研究表明 ZAR1 可用于提高猕猴桃对 Psa 的抗性，并揭示了效应子触发免疫和效应子触发毒力的先前未知的复杂性。
