Empty pericarp7 encodes a mitochondrial E–subgroup pentatricopeptide repeat protein that is required for ccmF_N editing, mitochondrial function and seed development in maize

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Abstract

Summary RNA editing, converting cytidines (C) to uridines (U) at specific sites in the transcripts of mitochondria and plastids, plays a critical role in organelle gene expression in land plants. Recently pentatricopeptide repeat ( PPR ) proteins were identified as site‐specific recognition factors for RNA editing. In this study, we characterized an empty pericarp7 mutant ( emp7 ) in Zea mays (maize), which confers an embryo‐lethal phenotype. In emp7 mutants, mitochondrial functions are seriously perturbed, resulting in a strikingly reduced respiration rate. Emp7 encodes an E–subgroup PPR protein that is localized exclusively in the mitochondrion. Null mutation of Emp7 abolishes the C → U editing of ccm F N transcript solely at position 1553. Ccm F N is coding for a subunit of heme lyase complex in the cytochrome c maturation pathway. The resulting Phe → Ser substitution in Ccm F N leads to the loss of Ccm F N protein and a strikingly reduced c ‐type cytochrome. Consequently, the mitochondrial cytochrome‐linked respiratory chain is impaired as a result of the disassembly of complex III in the emp7 mutant. These results indicate that the PPR –E subgroup protein EMP 7 is required for C → U editing of ccm F N ‐ 1553 at a position essential for cytochrome c maturation and mitochondrial oxidative phosphorylation, and hence is essential to embryo and endosperm development in maize.

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