| Categories genes  | Tags pericarp  growth  seed development  endosperm  seed  mitochondria 
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    • Here, we report the molecular characterization of the empty pericarp5 (emp5) mutants in maize (Zea mays)
    • EMP5 knockdown expression in transgenics resulted in slow growth and defective seeds
    • These results demonstrate that Emp5 encodes a PPR-DYW protein that is required for the editing of multiple transcripts in mitochondria, and the editing events, particularly the C-to-U editing at the rpl16-458 site, are critical to the mitochondrial functions and, hence, to seed development in maize
    • Null mutation of Emp5 results in abortion of embryo and endosperm development at early stages
    • Analysis of the mitochondrial transcripts revealed that loss of the EMP5 function abolishes the C-to-U editing of ribosomal protein L16 at the rpl16-458 site (100% edited in the wild type), decreases the editing at nine sites in NADH dehydrogenase9 (nad9), cytochrome c oxidase3 (cox3), and ribosomal protein S12 (rps12), and surprisingly increases the editing at five sites of ATP synthase F0 subunit a (atp6), apocytochrome b (cob), nad1, and rpl16
    • Analysis of the ortholog in rice (Oryza sativa) indicates that rice EMP5 has a conserved function in C-to-U editing of the rice mitochondrial rpl16-458 site
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