Mitochondria,the main energy transducers in plant cells,require the proper assembly of respiratory chain complexes Ⅰ-Ⅴ for their function.The NADH dehydrogenase 4,(nad4) gene encodes mitochondrial respiratory chain complex Ⅰ subunit Ⅳ,but the mechanism underlying nad4transcript splicing is unclear.Here,we report that the P-type pentatricopeptide repeat (PPR) protein DEFECTIVE KERNEL 43 (DEK43) is responsible for cis-splicing of the nad4 transcript in maize.We demonstrate that DEK43localizes to both the nucleus and mitochondria.The mutation of Dek43 resulted in embryo-lethal and light-colored defective kels.Among the 22 mitochondrial group Ⅱintrons,the splicing efficiency of nad4 introns 1 and 3 was reduced by up to 50％ compared to the wild type.The levels of complex Ⅰ and supercomplex Ⅰ+Ⅲ2 were also reduced in dek43.Furthermore,in-gel NADH dehydrogenase assays indicated that the activities of these complexes were significantly reduced in dek43.Further,the mitochondrial ultrastructure was altered in the mutant.Together,our findings indicate that DEK43,a dual-localized PPR protein,plays an important role in maintaining mitochondrial function and maize kel development.