The Pentatricopeptide Repeat Protein OTP87 Is Essential for RNA Editing of nad7 and atp1 Transcripts in Arabidopsis Mitochondria

被引:77
作者
Hammani, Kamel [1 ,2 ]
des Francs-Small, Catherine Colas [1 ]
Takenaka, Mizuki [4 ]
Tanz, Sandra K. [1 ]
Okuda, Kenji [3 ]
Shikanai, Toshiharu [3 ]
Brennicke, Axel [4 ]
Small, Ian [1 ]
机构
[1] Univ Western Australia, Australian Res Council, Ctr Excellence Plant Energy Biol, Crawley, WA 6009, Australia
[2] Univ Strasbourg, CNRS, Inst Biol Mol Plantes, F-67084 Strasbourg, France
[3] Kyoto Univ, Grad Sch Sci, Dept Bot, Kyoto 6068502, Japan
[4] Univ Ulm, D-89069 Ulm, Germany
基金
澳大利亚研究理事会;
关键词
CIS-ACTING ELEMENTS; PPR PROTEIN; CHLOROPLAST TRANSCRIPTS; COMPARATIVE GENOMICS; ELECTRON-TRANSPORT; MULTIPLE SITES; MESSENGER-RNA; DYW PROTEIN; IDENTIFICATION; RECOGNITION;
D O I
10.1074/jbc.M111.230516
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In plant organelles, RNA editing is a post-transcriptional mechanism that converts specific cytidines to uridines in RNA of both mitochondria and plastids, altering the information encoded by the gene. The cytidine to be edited is determined by a cis-element surrounding the editing site that is specifically recognized and bound by a trans-acting factor. All the trans-acting editing factors identified so far in plant organelles are members of a large protein family, the pentatricopeptide repeat (PPR) proteins. We have identified the Organelle Transcript Processing 87 (OTP87) gene, which is required for RNA editing of the nad7-C24 and atp1-C1178 sites in Arabidopsis mitochondria. OTP87 encodes an E-subclass PPR protein with an unusually short E-domain. The recombinant protein expressed in Escherichia coli specifically binds to RNAs comprising 30 nucleotides upstream and 10 nucleotides downstream of the nad7-C24 and atp1-C1178 editing sites. The loss-of-function of OTP87 results in small plants with growth and developmental delays. In the otp87 mutant, the amount of assembled respiratory complex V (ATP synthase) is highly reduced compared with the wild type suggesting that the amino acid alteration in ATP1 caused by loss of editing at the atp1-C1178 site affects complex V assembly in mitochondria.
引用
收藏
页码:21361 / 21371
页数:11
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