The pentatricopeptide repeat protein EMP9 is required for mitochondrial ccmB and rps4 transcript editing, mitochondrial complex biogenesis and seed development in maize
The pentatricopeptide repeat protein EMP9 is required for mitochondrial ccmB and rps4 transcript editing, mitochondrial complex biogenesis and seed development in maize
复制标题
五肽重复蛋白 EMP9 是玉米线粒体 ccmB 和 rps4 转录本编辑、线粒体复合物生物发生和种子发育所必需的
DOI:
10.1111/nph.14424
复制
发表时间:
2017
期刊:
影响因子:
9.4
通讯作者:
Tan Bao-Cai
中科院分区:
文献类型:
--
作者:
Yang Yan-Zhuo;Ding Shuo;Wang Hong-Chun;Sun Feng;Huang Wen-Long;Song Shu;Xu Chunhui;Tan Bao-Cai
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 anempty pericarp9(emp9) mutant in maize (Zea mays), we defined the functions of EMP9 in mitochondrial RNA editing, respiratory complex formation and seed development.Muinsertions in different regions ofEmp9facilitated dissection of the domain functions of the EMP9. 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 EMP9.Emp9encodes an E+ subclass PPR protein that is localized in mitochondria. Loss of EMP9 function abolishes the C‐to‐U editing ofccmB‐43 andrps4‐335 sites in mitochondria. The loss of editing atccmB‐43 andrps4‐335 affects the maturation of cytochromecand 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.