Plant immunity is activated upon pathogen perception and often affects growth and yield when it is constitutively active. How plants fine-tune immune homeostasis in their natural habitats remains elusive. Here, we discover a conserved immune suppression network in cereals that orchestrates immune homeostasis, centering on a Ca²⁺-sensor, RESISTANCE OF RICE TO DISEASES1 (ROD1). ROD1 promotes reactive oxygen species (ROS) scavenging by stimulating catalase activity, and its protein stability is regulated by ubiquitination. ROD1 disruption confers resistance to multiple pathogens, whereas a natural ROD1 allele prevalent in indica rice with agroecology-specific distribution enhances resistance without yield penalty. The fungal effector AvrPiz-t structurally mimics ROD1 and activates the same ROS-scavenging cascade to suppress host immunity and promote virulence. We thus reveal a molecular framework adopted by both host and pathogen that integrates Ca²⁺ sensing and ROS homeostasis to suppress plant immunity, suggesting a principle for breeding disease-resistant, high-yield crops.

植物免疫在病原体感知时被激活，并且当其组成型活跃时通常会影响生长和产量。植物如何在其自然栖息地微调免疫稳态仍然难以捉摸。在这里，我们在谷物中发现了一个保守的免疫抑制网络，该网络协调免疫稳态，以 Ca ²⁺传感器为中心，即水稻对疾病的抗性 1 (ROD1)。ROD1 通过刺激过氧化氢酶活性促进活性氧 (ROS) 清除，其蛋白质稳定性受泛素化调节。ROD1 破坏赋予对多种病原体的抗性，而在籼稻中普遍存在的天然ROD1等位基因具有农业生态特异性分布的水稻增强了抗性而不会降低产量。真菌效应器 AvrPiz-t 在结构上模仿 ROD1 并激活相同的 ROS 清除级联以抑制宿主免疫并促进毒力。因此，我们揭示了宿主和病原体采用的一种分子框架，该框架整合了 Ca ²⁺感应和 ROS 稳态来抑制植物免疫，为培育抗病高产作物提供了一条原则。