Hemara Lauren M, Chatterjee Abhishek, Yeh Shin-Mei, Chen Ronan K Y, Hilario Elena, Lievre Liam Le, Crowhurst Ross N, Bohne Deborah, Arshed Saadiah, Patterson Haileigh R, Barrett-Manako Kelvina, Thomson Susan, Allan Andrew C, Brendolise Cyril, Chagné David, Templeton Matthew D, Tahir Jibran, Jayaraman Jay
School of Biological Sciences, The University of Auckland, Auckland, New Zealand.
The New Zealand Institute for Plant and Food Research Limited, Mount Albert Research Centre, New Zealand.
Plant Cell Environ. 2025 Feb;48(2):1037-1050. doi: 10.1111/pce.15189. Epub 2024 Oct 13.
Pseudomonas syringae pv. actinidiae biovar 3 (Psa3) has decimated kiwifruit orchards growing susceptible kiwifruit Actinidia chinensis varieties. Effector loss has occurred recently in Psa3 isolates from resistant kiwifruit germplasm, resulting in strains capable of partially overcoming resistance present in kiwiberry vines (Actinidia arguta, Actinidia polygama, and Actinidia melanandra). Diploid male A. melanandra recognises several effectors, sharing recognition of at least one avirulence effector (HopAW1a) with previously studied tetraploid kiwiberry vines. Sequencing and assembly of the A. melanandra genome enabled the characterisation of the transcriptomic response of this non-host to wild-type and genetic mutants of Psa3. A. melanandra appears to mount a classic effector-triggered immunity (ETI) response to wildtype Psa3 V-13, as expected. Surprisingly, the type III secretion (T3SS) system-lacking Psa3 V-13 ∆hrcC strain did not appear to trigger pattern-triggered immunity (PTI) despite lacking the ability to deliver immunity-suppressing effectors. Contrasting the A. melanandra responses to an effectorless Psa3 V-13 ∆33E strain and to Psa3 V-13 ∆hrcC suggested that PTI triggered by Psa3 V-13 was based on the recognition of the T3SS itself. The characterisation of both ETI and PTI branches of innate immunity responses within A. melanandra further enables breeding for durable resistance in future kiwifruit cultivars.
猕猴桃溃疡病菌3号生物变种（Psa3）已使种植易感中华猕猴桃品种的果园遭受重创。最近，从抗性猕猴桃种质中分离出的Psa3菌株出现了效应子缺失现象，从而产生了能够部分克服软枣猕猴桃藤蔓（软枣猕猴桃、葛枣猕猴桃和黑蕊猕猴桃）中存在的抗性的菌株。二倍体雄性黑蕊猕猴桃识别多种效应子，与之前研究的四倍体软枣猕猴桃藤蔓共享对至少一种无毒效应子（HopAW1a）的识别。黑蕊猕猴桃基因组的测序和组装使得能够对该非寄主对Psa3野生型和基因突变体的转录组反应进行表征。正如预期的那样，黑蕊猕猴桃似乎对野生型Psa3 V-13产生了经典的效应子触发免疫（ETI）反应。令人惊讶的是，尽管缺乏递送抑制免疫效应子的能力，但缺乏III型分泌（T3SS）系统的Psa3 V-13 ∆hrcC菌株似乎并未触发模式触发免疫（PTI）。将黑蕊猕猴桃对无效应子的Psa3 V-13 ∆33E菌株和对Psa3 V-13 ∆hrcC菌株的反应进行对比表明，Psa3 V-13触发的PTI是基于对T3SS本身的识别。对黑蕊猕猴桃先天免疫反应中ETI和PTI分支的表征进一步有助于未来猕猴桃品种的持久抗性育种。
