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
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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
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发表时间:
2017
期刊:
影响因子:
9.4
通讯作者:
Tan Bao-Cai
Tan Bao-Cai
中科院分区:
生物学1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

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五肽重复 (PPR) 蛋白包含陆地植物中一系列序列特异性 RNA 结合蛋白。由于其家族规模较大且突变体中频繁发生胚胎致死,许多 PPR 蛋白的分子功能和生理作用尚不清楚。通过对玉米(Zea mays)中空果皮9(emp9)突变体的表征,我们定义了EMP9在线粒体RNA编辑、呼吸复合体形成和种子发育中的功能。Emp9不同区域的Mu插入有利于EMP9域功能的剖析。通过对多个等位基因的遗传和功能分析,我们发现两个N端PPR基序和部分E+结构域的缺失并不能消除EMP9的编辑功能。Emp9编码位于线粒体中的E+亚类PPR蛋白。 EMP9 功能的丧失会消除线粒体中 ccmB-43 和 rps4-335 位点的 C-to-U 编辑。 atccmB-43 和rps4-335 编辑的丢失会影响细胞色素Cand 的成熟,从而损害线粒体呼吸复合物,特别是复合物 III 的生物发生。这项工作扩展了我们对 PPR-E+ 蛋白在编辑功能和种子发育中的理解,并为高等植物中线粒体 CcmB 蛋白的分子功能提供了见解。
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.