In plants, pathogen effector-triggered immunity (ETI) often leads to programmed cell death, which is restricted by NPR1, an activator of systemic acquired resistance. However, the biochemical activities of NPR1 enabling it to promote defense and restrict cell death remain unclear. Here we show that NPR1 promotes cell survival by targeting substrates for ubiquitination and degradation through formation of salicylic acid-induced NPR1 condensates (SINCs). SINCs are enriched with stress response proteins, including nucleotide-binding leucine-rich repeat immune receptors, oxidative and DNA damage response proteins, and protein quality control machineries. Transition of NPR1 into condensates is required for formation of the NPR1-Cullin 3 E3 ligase complex to ubiquitinate SINC-localized substrates, such as EDS1 and specific WRKY transcription factors, and promote cell survival during ETI. Our analysis of SINCs suggests that NPR1 is centrally integrated into the cell death or survival decisions in plant immunity by modulating multiple stress-responsive processes in this quasi-organelle.

在植物中，病原体效应触发的免疫 (ETI) 通常会导致程序性细胞死亡，这受到 NPR1（一种全身获得性抗性激活剂）的限制。然而，NPR1 的生化活性使其能够促进防御和限制细胞死亡仍不清楚。在这里，我们表明 NPR1 通过形成水杨酸诱导的 NPR1 缩合物（SINC）靶向底物进行泛素化和降解来促进细胞存活。SINC 富含应激反应蛋白，包括核苷酸结合的富含亮氨酸的重复免疫受体、氧化和 DNA 损伤反应蛋白以及蛋白质质量控​​制机制。NPR1 转变为缩合物是形成 NPR1-Cullin 3 E3 连接酶复合物以泛素化 SINC 定位底物（例如 EDS1 和特定的 WRKY 转录因子）所必需的，并促进 ETI 期间的细胞存活。我们对 SINC 的分析表明，NPR1 通过调节这种准细胞器中的多个应激反应过程，集中整合到植物免疫中的细胞死亡或存活决策中。