The intracellular plant resistance (R) proteins, nucleotide-binding and leucine-rich repeat (NLR) proteins, mediate resistance to pathogens by enabling recognition and rapid response. The response consists of the induction of a defensive suite that typically culminates in the hypersensitive response (HR), death of the plant cells at and around an infection site. The Arabidopsis intracellular innate immune receptor protein RESISTANCE TO PSEUDOMONAS MACULICOLA1 (RPM1) is a coiled-coil (CC) type of NLR protein that specifies resistance to strains of the bacterial pathogen Pseudomonas syringae expressing the type III effector proteins AvrRpm1 and AvrB. We previously demonstrated that RPM1-myc (an epitope-tagged version of RPM1) disappears coincident with the onset of HR induced by AvrRpm1. Infection with P. syringae expressing two other type III effector proteins, AvrRpt2 and AvrRps4, also initiated RPM1-myc disappearance at time points coincident with the HR they initiate through the NLR proteins RESISTANCE TO P. SYRINGAE2 (RPS2) and RESISTANCE TO P. SYRINGAE 4 (RPS4), respectively. Here, we use mutants impaired in NLR gene dependent signaling to demonstrate that disappearance of RPM1-myc requires normal NLR gene dependent signaling steps, but does not require HR. Inhibitors of the 26S proteasome block the disappearance of RPM1-myc and enhance RPM1-myc-dependent cell death. Our data are consistent with a model in which RPM1 is degraded by the 26S proteasome to limit the extent of RPM1-dependent signaling and/or cell death. Furthermore, AvrRpt2 induces disappearance of RPM1-myc in rps2 mutant plants without HR, suggesting that RPM1 is part of the host target of the virulence activity of AvrRpt2.

细胞内植物抗性（R）蛋白，核苷酸结合和富含亮氨酸的重复（NLR）蛋白通过实现识别和快速响应来介导对病原体的抗性。该反应包括诱导防御性套装，该防御性套装通常最终导致超敏反应（HR），感染部位及其周围植物细胞死亡。在拟南芥细胞内的天然免疫受体蛋白质的抗假单胞菌MACULICOLA1（RPM1）是NLR蛋白的指定抗细菌病原体的菌株卷曲螺旋（CC）类型丁香假单胞菌表达III型效应蛋白AvrRpm1和AvrB。我们先前证明，RPM1-myc（RPM1的表位标记版本）消失与由AvrRpm1诱导的HR发生同时发生。表达另外两种III型效应蛋白AvrRpt2和AvrRps4的丁香假单胞菌感染也引发RPM1-myc消失，时间点与它们通过NLR蛋白产生的HR一致，即对P. SYRINGAE2（RPS2）和对P. SYRINGAE的抵抗4（RPS4）。在这里，我们使用在NLR基因依赖性信号传导中受损的突变体来证明RPM1-myc的消失需要正常的NLR基因依赖性信号转导步骤，但不需要HR。26S蛋白酶体抑制剂可阻止RPM1-myc的消失并增强RPM1-myc依赖性细胞死亡。我们的数据与一个模型一致，其中RPM1被26S蛋白酶体降解以限制RPM1依赖性信号传导和/或细胞死亡的程度。此外，AvrRpt2诱导没有HR的rps2突变植物中RPM1-myc的消失，表明RPM1是AvrRpt2毒力活性宿主目标的一部分。