School of Municipal and Environmental Engineering, Shandong Jianzhu University, Jinan, China.
Plant Signal Behav. 2011 Jun;6(6):794-9. doi: 10.4161/psb.6.6.15143. Epub 2011 Jun 1.
Two layers of plant immune systems are used by plants to defend against phytopathogens. The first layer is pathogen-associate molecular patterns (PAMPs)-triggered immunity (PTI), which is activated by plant cell-surface pattern recognition receptors (PRRs) upon perception of microbe general elicitors. The second layer is effector-triggered immunity (ETI), which is initiated by specific recognition of pathogen type III secreted effectors (T3SEs) with plant intracellular resistance (R) proteins. Current opinions agree that ETI was evolved from PTI, and the impetus for the evolution of plant immunity is pathogen T3SEs, which exhibit virulence functions through blocking PTI, but show avirulence functions for triggering ETI. A Decoy Model was put forward and explained that the avirulence targets of pathogen T3SEs were evolved as decoys to compete with the virulence targets for binding with pathogen T3SEs. However, little direct evidence for the evolutionary mode has been offered. Here, we reviewed the recent progresses about Pto, PBS1, and RIN4 to present our viewpoints about the evolution of plant immunity.
植物利用两层免疫系统来抵御植物病原体。第一层是病原体相关分子模式（PAMPs）触发的免疫（PTI），当植物细胞表面模式识别受体（PRRs）感知到微生物的一般激发子时，就会被激活。第二层是效应物触发的免疫（ETI），它是由植物细胞内的抗性（R）蛋白对病原体 III 型分泌效应物（T3SEs）的特异性识别启动的。目前的观点认为，ETI 是从 PTI 进化而来的，而植物免疫进化的动力是病原体 T3SEs，它们通过阻断 PTI 表现出毒性功能，但通过触发 ETI 表现出无毒功能。提出了一个诱饵模型，并解释了病原体 T3SEs 的无毒靶标是如何进化为诱饵，与毒性靶标竞争与病原体 T3SEs 的结合。然而，对于这种进化模式，几乎没有直接的证据。在这里，我们回顾了最近关于 Pto、PBS1 和 RIN4 的进展，提出了我们对植物免疫进化的观点。
