Key Laboratory of South China Agricultural Plant Molecular Analysis and Genetic Improvement & Guangdong Provincial Key Laboratory of Applied Botany, South China Botanical Garden, Chinese Academy of Sciences, Guangzhou, China.
University of Chinese Academy of Sciences, Beijing, China.
Plant Cell. 2021 Mar 22;33(1):153-171. doi: 10.1093/plcell/koaa007.
Plants have evolved precise mechanisms to optimize immune responses against pathogens. ENHANCED DISEASE SUSCEPTIBILITY 1 (EDS1) plays a vital role in plant innate immunity by regulating basal resistance and effector-triggered immunity. Nucleocytoplasmic trafficking of EDS1 is required for resistance reinforcement, but the molecular mechanism remains elusive. Here, we show that EDS1-INTERACTING J PROTEIN1 (EIJ1), which acts as a DnaJ protein-like chaperone in response to pathogen infection, functions as an essential negative regulator of plant immunity by interacting with EDS1. The loss-of-function mutation of EIJ1 did not affect plant growth but significantly enhanced pathogen resistance. Upon pathogen infection, EIJ1 relocalized from the chloroplast to the cytoplasm, where it interacted with EDS1, thereby restricting pathogen-triggered trafficking of EDS1 to the nucleus and compromising resistance at an early infection stage. During disease development, EIJ1 was gradually degraded, allowing the nuclear accumulation of EDS1 for transcriptional resistance reinforcement. The avirulent strain Pst DC3000 (AvrRps4) abolished the repressive action of EIJ1 by rapidly inducing its degradation in the effector-triggered immunity response. Thus, our findings show that EIJ1 is an essential EDS1-dependent negative regulator of innate plant immunity and provide a mechanistic understanding of how the nuclear versus cytoplasmic distribution of EDS1 is regulated during the immune response.
植物已经进化出精确的机制来优化对病原体的免疫反应。增强疾病敏感性 1（EDS1）通过调节基础抗性和效应器触发的免疫在植物先天免疫中发挥着至关重要的作用。EDS1 的核质转运对于增强抗性是必需的，但分子机制仍不清楚。在这里，我们表明，EDS1-INTERACTING J PROTEIN1（EIJ1）作为一种 DnaJ 蛋白样伴侣，在受到病原体感染时发挥作用，通过与 EDS1 相互作用，作为植物免疫的必需负调节剂。EIJ1 的功能丧失突变不影响植物生长，但显著增强了病原体的抗性。在病原体感染时，EIJ1 从叶绿体重新定位到细胞质，在细胞质中与 EDS1 相互作用，从而限制了病原体触发的 EDS1 向细胞核的转运，并在早期感染阶段损害了抗性。在疾病发展过程中，EIJ1 逐渐降解，允许 EDS1 在核内积累，以增强转录抗性。无毒菌株 Pst DC3000（AvrRps4）通过在效应器触发的免疫反应中迅速诱导其降解，从而消除了 EIJ1 的抑制作用。因此，我们的研究结果表明，EIJ1 是一种必需的 EDS1 依赖性植物先天免疫负调节剂，并提供了对 EDS1 在免疫反应过程中如何调控核质分布的机制理解。
