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As one of the best-studied RNA binding proteins in plant, pentatricopeptide repeats (PPRs) protein are mainly targeted to mitochondria and/or chloroplasts for RNA processing to regulate the biogenesis and function of the organelles, but its molecular mechanism and role in development remain to be further revealed. Here, we identified a mitochondria-localized P-type small PPR protein, MITOCHONDRION-MEDIATED GROWTH DEFECT 1 (MID1) that is crucial for  Arabidopsis  development. Mutation in  MID1  causes retarded embryo development and stunted plant growth with defects in cell expansion and proliferation. Molecular experiments showed that  MID1  is required for the splicing of the  nad2  intron 1 in mitochondria. Consistently,  mid1  plants display significant reduction in the abundance and activity of mitochondrial respiration complex I, accompanied by abnormal mitochondrial morphology and energy metabolism. Furthermore, MID1 is associated with other  trans -factors involved in  NICOTINAMIDE ADENINE DINUCLEOTIDE HYDROGEN  ( NADH )  DEHYDROGENASE SUBUNIT 2  ( nad2 ) intron 1 splicing, and interacts directly with itself and MITOCHONDRIAL STABILITY FACTOR 1 (MTSF1). This suggests that MID1 most likely functions as a dimer for  nad2  intron 1 splicing. Together, we characterized a novel PPR protein MID1 for  nad2  intron 1 splicing.

Pentatricopeptide repeat protein MID1 modulates nad2 intron 1 splicing and Arabidopsis development