The mitochondrial pentatricopeptide repeat protein EMP12 is involved in the splicing of three nad2 introns and seed development in maize.

Abstract

Plant mitochondrial genes contain cis- and trans-group II introns that must be spliced before translation. The mechanism by which these introns are spliced is not well understood. Several families of proteins have been implicated in the intron splicing, of which the pentatricopeptide repeat (PPR) proteins are proposed to confer the substrate binding specificity. However, very few PPRs are characterized. Here, we report the function of a P-type PPR protein, EMP12, and its role in seed development. EMP12 is targeted to mitochondria. Loss-of-function mutation in Emp12 severely arrests embryo and endosperm development, causing embryo lethality. The trans-splicing of mitochondrial nad2 intron 2 and cis-splicing of nad2 intron 4 are abolished, whereas the cis-splicing of nad2 intron 1 is reduced in emp12 mutants. As a result, complex I assembly is disrupted, and its activity is strongly reduced in the mutants. The expression of the alternative oxidase and several components of other mitochondrial complexes is increased, possibly in response to the defective complex I. These results suggest that Emp12 is required for the trans-splicing of nad2 intron 2 and cis-splicing of nad2 introns 1 and 4, and is important to complex I biogenesis, and embryogenesis and endosperm development in maize.