A fungal effector targets a heat shock-dynamin protein complex to modulate mitochondrial dynamics and reduce plant immunity.

Abstract

Mitochondria are essential for animal and plant immunity. Here, we report that the effector MoCDIP4 of the fungal pathogen <i>Magnaporthe oryzae</i> 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 <i>OsDjA9</i> or overexpression of <i>OsDRP1E</i> or <i>MoCDIP4</i> in transgenic rice results in shortened mitochondria and enhanced susceptibility to <i>M. oryzae</i> Overexpression of <i>OsDjA9</i> or knockout of <i>OsDRP1E</i> in transgenic rice, in contrast, leads to elongated mitochondria and enhanced resistance to <i>M. oryzae</i> 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.