Plant effector-triggered immunity requires RNA helicase PMH2-mediated group II intron splicing in mitochondria.

Abstract

In plants, reactive oxygen species (ROS) play a crucial role in rapidly responding to biotic stresses, thus contributing to the establishment of immune networks and plant resistance against pathogen attack. The 2-layered plant immune system consists of the cell-surface pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and intracellular effector-triggered immunity (ETI), both of which are associated with ROS burst. Mitochondria, serving as a major source of intracellular ROS, are key to plant immunity, and their function depends on the RNA processing of mitochondrial genes. The DEAD-box RNA helicase PUTATIVE MITOCHONDRIAL RNA HELICASE 2 (PMH2) is required for efficient group II intron splicing in mitochondria; however, how PMH2-mediated fine RNA splicing contributes to plant immunity remains unknown. Here, we revealed the function of PMH2 in ETI using Arabidopsis thaliana. ETI activation led to the PMH2-mediated reduction in splicing efficiency of cox2, which encodes the subunit of mitochondrial respiratory chain complex IV, and the activity of complex IV, thereby promoting the generation of mtROS. Moreover, PMH2-mediated mtROS facilitated the expression of the nuclear immunity genes. These results collectively suggest that PMH2 contributes to specific mitochondrial RNA splicing and fine-tunes the mitochondrial ROS burst, therefore maintaining robust plant immunity. Our study provides the mechanism of RNA helicase linking RNA processing and mitochondrial dynamics to plant ETI.