Mitochondria are essential for animal and plant immunity. Here, we report that the effector MoCDIP4 of the fungal pathogen Magnaporthe oryzae targets the mitochondria-associated OsDjA9-OsDRP1E protein complex to reduce rice immunity. The DnaJ protein OsDjA9 interacts with the dynamin-related protein OsDRP1E and promotes the degradation of OsDRP1E, which functions in mitochondrial fission. By contrast, MoCDIP4 binds OsDjA9 to compete with OsDRP1E, resulting in OsDRP1E accumulation. Knockout of OsDjA9 or overexpression of OsDRP1E or MoCDIP4 in transgenic rice results in shortened mitochondria and enhanced susceptibility to M. oryzae. Overexpression of OsDjA9 or knockout of OsDRP1E in transgenic rice, in contrast, leads to elongated mitochondria and enhanced resistance to M. oryzae. Our study therefore reveals a previously unidentified pathogen-infection strategy in which the pathogen delivers an effector into plant cells to target an HSP40-DRP complex; the targeting leads to the perturbation of mitochondrial dynamics, thereby inhibiting mitochondria-mediated plant immunity.

线粒体对动植物免疫至关重要。在这里，我们报告了真菌病原体稻瘟病菌的效应子 MoCDIP4靶向线粒体相关的 OsDjA9-OsDRP1E 蛋白复合物以降低水稻免疫力。DnaJ 蛋白 OsDjA9 与 dynamin 相关蛋白 OsDRP1E 相互作用并促进 OsDRP1E 的降解，后者在线粒体裂变中起作用。相比之下，MoCDIP4 结合 OsDjA9 与 OsDRP1E 竞争，导致 OsDRP1E 积累。在转基因水稻中敲除OsDjA9或过表达OsDRP1E或MoCDIP4会导致线粒体缩短并增强对米杆菌的易感性。OsDjA9的过表达或敲除相反，转基因水稻中的OsDRP1E会导致线粒体延长并增强对稻瘟病菌的抗性。因此，我们的研究揭示了一种以前未知的病原体感染策略，其中病原体将效应物传递到植物细胞中以靶向 HSP40-DRP 复合物。靶向导致线粒体动力学的扰动，从而抑制线粒体介导的植物免疫。