A mitochondrial pentatricopeptide repeat protein enhances cold tolerance by modulating mitochondrial superoxide in rice

Cold stress affects rice growth and productivity. Defects in the plastid-localized pseudouridine synthase OsPUS1 affect chloroplast ribosome biogenesis, leading to low-temperature albino seedlings and accumulation of reactive oxygen species (ROS). Here, we report an ospus1-1 suppressor, sop10 . SOP10 encodes a mitochondria-localized pentatricopeptide repeat protein. Mutations in SOP10 impair intron splicing of the nad4 and nad5 transcripts and decrease RNA editing efficiency of the nad2 , nad6 , and rps4 transcripts, resulting in deficiencies in mitochondrial complex I, thus decrease ROS generation and rescuing the albino phenotype. Overexpression of different compartment-localized superoxide dismutases (SOD) genes in ospus1-1 reverses the ROS over-accumulation and albino phenotypes to various degrees, with Mn-SOD reversing the best. Mutation of SOP10 in indica rice varieties enhances cold tolerance with lower ROS levels. We find that the mitochondrial superoxide plays a key role in rice cold responses, and identify a mitochondrial superoxide modulating factor, informing efforts to improve rice cold tolerance. Cold stress hampers rice growth and yield. This paper demonstrates that mitochondrial superoxide plays a key role in cold responses, and identifies a pentatricopeptide repeat protein which modulates mitochondrial superoxide and rice cold tolerance.