EMP32 is required for the -splicing of intron 2 and seed development in maize.

Pentatricopeptide repeat (PPR) proteins play an important role in post-transcriptional regulation of mitochondrial gene expression. Functions of many PPR proteins and their roles in plant growth and development remain unknown. Through characterization of an () mutant, we identified the function of in mitochondrial intron splicing and seed development in maize. The loss-of-function mutant shows embryo lethality with severely arrested embryo and endosperm development, and over-expression of rescues the embryo-lethality. EMP32 is a P-type PPR protein targeted to mitochondria. Loss of function in dramatically decreases the splicing efficiency of intron 2, while complementation of restores the splicing efficiency. Although intron 2 is partially spliced in the wild type, over-expression of does not increase the splicing efficiency. The splicing deficiency of intron 2 blocks the assembly of mitochondrial complex I and dramatically reduces its activity, which may explain the embryo-lethality in . In addition to the one copy of in the maize mitochondrial genome, we identified one to six copies of in the nuclear genomes in different maize inbred lines. These copies appear not to be expressed. Together, our results revealed that the P-type PPR protein EMP32 is required for the -splicing of intron 2 and seed development in maize.