Plant immunity is controlled by both positive regulators such as PBS3 and EDS1 and negative regulators such as NPR3 and NPR4. However, the relationships among these important immune regulators remain elusive. In this study, we found that PBS3 interacts with EDS1 in both the cytoplasm and the nucleus, and is required for EDS1 protein accumulation. NPR3 and NPR4, which function as salicylic acid receptors and adaptors of Cullin3-based E3 ligase, interact with and mediate the degradation of EDS1 via the 26S proteasome. We further discovered that PBS3 inhibits the polyubiquitination and subsequent degradation of EDS1 by reducing the association of EDS1 with the Cullin3 adaptors NPR3 and NPR4. Furthermore, we showed that PBS3 and EDS1 also contribute to PAMP-triggered immunity in addition to effector-triggered immunity. Collectively, our study reveals a novel mechanism by which plants fine-tune defense responses by inhibiting the degradation of a positive player in plant immunity.

植物免疫力受正调节剂（例如PBS3和EDS1）和负调节剂（例如NPR3和NPR4）的控制。但是，这些重要的免疫调节剂之间的关系仍然难以捉摸。在这项研究中，我们发现PBS3在细胞质和细胞核中都与EDS1相互作用，并且是EDS1蛋白积累所必需的。NPR3和NPR4作为水杨酸受体和基于Cullin3的E3连接酶的衔接子，通过26S蛋白酶体与EDS1相互作用并介导EDS1的降解。我们进一步发现，PBS3通过减少EDS1与Cullin3衔接子NPR3和NPR4的结合来抑制EDS1的多聚泛素化和随后的降解。此外，我们表明PBS3和EDS1除效应物触发的免疫力外，还有助于PAMP触发的免疫力。总的来说，