Plants use cell-surface immune receptors to recognize pathogen-specific patterns to evoke basal immunity. ENHANCED DISEASE SUSCEPTIBILITY (EDS1) is known to be crucial for plant basal immunity, whereas its activation mechanism by pattern recognition remains enigmatic. Here, we show that the fungal pattern chitin induced the plasma membrane-anchored receptor-like cytoplasmic kinase PBS1-LIKE 19 (PBL19) to undergo nuclear translocation in Arabidopsis. The palmitoylation-deficient PBL19^C3A variant constantly resided in the nucleus, triggering transcriptional self-amplification mainly through WRKY8 and EDS1-dependent constitutive immunity. Unexpectedly, the metacaspase-cleaved PBL19 lacking the N-terminal nuclear localization sequence specifically interacted with and phosphorylated EDS1 in the cytoplasm. Phosphodeficient EDS1 attenuated PBL19^C3A-induced constitutive immunity, while phosphomimetic EDS1 complemented the loss of PBL19 for fungal resistance. Collectively, these findings reveal a compelling model wherein the plasma membrane, nuclear and cytoplasmic pools of PBL19 temporally coordinate distinct roles of immune signal receiver, amplifier and effector to boost plant antifungal immunity via EDS1.

植物使用细胞表面免疫受体来识别病原体特异性模式以唤起基础免疫。已知增强的疾病易感性（EDS1）对植物基础免疫至关重要，而其通过模式识别的激活机制仍然是个谜。在这里，我们表明真菌模式几丁质诱导质膜锚定受体样细胞质激酶 PBS1-LIKE 19 (PBL19) 在拟南芥中进行核易位。棕榈酰化缺陷型 PBL19 ^C3A变体持续存在于细胞核中，主要通过 WRKY8 和 EDS1 依赖性组成免疫触发转录自我扩增。出乎意料的是，缺乏 N 末端核定位序列的间半胱天冬酶切割的 PBL19 与细胞质中的 EDS1 特异性相互作用并使其磷酸化。磷缺乏 EDS1 减弱了 PBL19 ^C3A诱导的组成性免疫，而磷模拟 EDS1 补充了 PBL19 对真菌抗性的损失。总的来说，这些发现揭示了一个令人信服的模型，其中 PBL19 的质膜、核和细胞质池在时间上协调免疫信号接收器、放大器和效应器的不同作用，以通过 EDS1 增强植物抗真菌免疫。