Department of Energy Plant Research Laboratory, Michigan State University, East Lansing, MI 48824, USA.
Proc Natl Acad Sci U S A. 2011 Jun 28;108(26):10774-9. doi: 10.1073/pnas.1103338108. Epub 2011 Jun 13.
Innate immunity in plants can be triggered by microbe- and pathogen-associated molecular patterns. The pathogen-associated molecular pattern-triggered immunity (PTI) is often suppressed by pathogen effectors delivered into the host cell. Plants can overcome pathogen suppression of PTI and reestablish pathogen resistance through effector-triggered immunity (ETI). An unanswered question is how plants might overcome pathogen-suppression of PTI during ETI. Findings described in this paper suggest a possible mechanism. During Pseudomonas syringae pathovar tomato (Pst) DC3000 infection of Arabidopsis, a host ADP ribosylation factor guanine nucleotide exchange factor, AtMIN7, is destabilized by the pathogen effector HopM1 through the host 26S proteasome. In this study, we discovered that AtMIN7 is required for not only PTI, consistent with the notion that Pst DC3000 degrades AtMIN7 to suppress PTI, but also ETI. The AtMIN7 level in healthy plants is low, but increases posttranscriptionally in response to activation of PTI. Whereas DC3000 infection led to degradation of AtMIN7, activation of ETI by three different effectors, AvrRpt2, AvrPphB, and HopA1, in Col-0 plants blocks the ability of Pst DC3000 to destabilize AtMIN7. Further analyses of bacterial translocation of HopM1 and AtMIN7 stability in HopM1 transgenic plants show that ETI prevents HopM1-mediated degradation of AtMIN7 inside the plant cell. Both AtMIN7 and HopM1 are localized to the trans-Golgi network/early endosome, a subcellular compartment that is not previously known to be associated with bacterial pathogenesis in plants. Thus, blocking pathogen degradation of trans-Golgi network/early endosome-associated AtMIN7 is a critical part of the ETI mechanism to counter bacterial suppression of PTI.
植物的先天免疫可以被微生物和病原体相关分子模式触发。病原体相关分子模式触发的免疫（PTI）经常被病原体效应物抑制。植物可以通过效应物触发的免疫（ETI）克服 PTI 的病原体抑制并重新建立病原体抗性。一个未解决的问题是植物如何在 ETI 期间克服 PTI 的病原体抑制。本文描述的研究结果提出了一种可能的机制。在丁香假单胞菌番茄亚种（Pst）DC3000 感染拟南芥期间，一种宿主 ADP 核糖基化因子鸟嘌呤核苷酸交换因子 AtMIN7 被病原体效应物 HopM1 通过宿主 26S 蛋白酶体稳定化。在这项研究中，我们发现 AtMIN7 不仅需要 PTI，这与 Pst DC3000 降解 AtMIN7 以抑制 PTI 的观点一致，还需要 ETI。健康植物中的 AtMIN7 水平较低，但在 PTI 激活后转录后增加。虽然 DC3000 感染导致 AtMIN7 降解，但 Col-0 植物中三种不同效应物 AvrRpt2、AvrPphB 和 HopA1 的 ETI 激活阻止了 Pst DC3000 破坏 AtMIN7 的能力。对 HopM1 的细菌易位和 HopM1 转基因植物中 AtMIN7 稳定性的进一步分析表明，ETI 阻止了 HopM1 介导的植物细胞内 AtMIN7 的降解。AtMIN7 和 HopM1 都定位于转高尔基网络/早期内体，该亚细胞区室以前不知道与植物中的细菌发病机制有关。因此，阻止病原体降解与转高尔基网络/早期内体相关的 AtMIN7 是 ETI 机制的一个关键部分，可对抗 PTI 的细菌抑制。
