Mitochondrial AtPAM16 is required for plant survival and the negative regulation of plant immunity.

Proteins containing nucleotide-binding and leucine-rich repeat domains (NB-LRRs) serve as immune receptors in plants and animals. Negative regulation of immunity mediated by NB-LRR proteins is crucial, as their overactivation often leads to autoimmunity. Here we describe a new mutant, snc1-enhancing (muse) forward genetic screen, targeting unknown negative regulators of NB-LRR-mediated resistance in Arabidopsis. From the screen, we identify MUSE5, which is renamed as AtPAM16 because it encodes the ortholog of yeast PAM16, part of the mitochondrial inner membrane protein import motor. Consistently, AtPAM16-GFP localizes to the mitochondrial inner membrane. AtPAM16L is a paralog of AtPAM16. Double mutant Atpam16-1 Atpam16l is lethal, indicating that AtPAM16 function is essential. Single mutant Atpam16 plants exhibit a smaller size and enhanced resistance against virulent pathogens. They also display elevated reactive oxygen species (ROS) accumulation. Therefore, AtPAM16 seems to be involved in importing a negative regulator of plant immunity into mitochondria, thus protecting plants from over-accumulation of ROS and preventing autoimmunity.