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The pentatricopeptide repeat protein EMP 9 is required for mitochondrial ccmB and rps4 transcript editing, mitochondrial complex biogenesis and seed development in maize
Author(s) -
Yang YanZhuo,
Ding Shuo,
Wang HongChun,
Sun Feng,
Huang WenLong,
Song Shu,
Xu Chunhui,
Tan BaoCai
Publication year - 2017
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/nph.14424
Subject(s) - pentatricopeptide repeat , biology , genetics , mitochondrial biogenesis , mutant , rna editing , biogenesis , mitochondrion , mitochondrial dna , gene , microbiology and biotechnology , computational biology , rna
Summary Pentatricopeptide repeat ( PPR ) proteins comprise a large family of sequence‐specific RNA binding proteins in land plants. Because of its large family size and frequent embryo lethality in the mutants, molecular functions and physiological roles of many PPR proteins are unknown. Through characterization of an empty pericarp9 ( emp9 ) mutant in maize ( Zea mays ), we defined the functions of EMP 9 in mitochondrial RNA editing, respiratory complex formation and seed development. Mu insertions in different regions of Emp9 facilitated dissection of the domain functions of the EMP 9. Through genetic and functional analyses of multiple alleles, we showed that deletions of two N‐terminal PPR motifs and partial E+ domain do not eliminate the editing function of EMP 9. Emp9 encodes an E+ subclass PPR protein that is localized in mitochondria. Loss of EMP 9 function abolishes the C‐to‐U editing of ccmB ‐43 and rps4 ‐335 sites in mitochondria. The loss of editing at ccmB ‐43 and rps4 ‐335 affects the maturation of cytochrome c and impairs the biogenesis of mitochondrial respiratory complexes, particularly complex III . This work extends our understanding of PPR ‐E+ protein in editing function and seed development, and provides insights into the molecular function of mitochondrial CcmB protein in higher plants.