rhe Mitochondrion-Targeted PENTATRICOPEPTIDE REPEAT78 Protein Is Required for nad5 Mature mRNA Stability and Development in Maize

作     者：Ya-Feng Zhang Masaharu Suzuki Feng Sun Bao-Cai Tan 

作者机构：Key Laboratory of Plant Cell Engineering and Germplasm Innovation Ministry of Education School of Life Sciences Shandong University Jinan 250100 China Guangdong Provincial Key Laboratory of Plant Molecular Breeding College of Agriculture South China Agricultural University Guangzhou 510642 China Plant Molecular and Cellular Biology Program University of Florida Gainesville Florida 32611 USA 

出 版 物：《Molecular Plant》 (分子植物（英文版）)

年 卷 期：2017年第10卷第10期

页      面：1321-1333页

核心收录：

学科分类：0710[理学-生物学] 071010[理学-生物化学与分子生物学] 081704[工学-应用化学] 07[理学] 08[工学] 0817[工学-化学工程与技术] 

基　　金：supported by grants to B.C.T. from the National Natural Science Foundation of China to Y.F.Z. from the National Natural Science Foundation of China 

主　　题：PPR nad5 mitochondrial RNA stability complex I seed development maize 

摘      要：Pentatricopepetide repeat （PPR） proteins are a large family of RNA-binding proteins involved in RNA meta- bolism in plant organelles. Although many PPR proteins have been functionally studied, few of them are identified with a function in mitochondrial RNA stability. By using a reverse genetic approach, we characterized the role of the mitochondrion-targeted PPR78 protein in nad5 mature mRNA stability and maize （Zea mays） seed development. Loss of PPR78 function leads to a dramatic reduction in the steady-state level of mitochondrial nad5 mature mRNA, blocks the assembly of complex I in the electron transport chain, and causes an arrest in embryogenesis and endosperm development. Characterization of a second strong allele confirms the function of PPR78 in nad5 mRNA accumulation and maize seed development. The generation of mature nad5 requires the assembly of three distinct precursor RNAs via transsplicing reactions, and the accumulation ofnad5T1 precursor is reduced in the ppr78 mutants. However, it is the instability of mature nad5 rather than nad5T1 causing loss of the full-length nad5 transcript, and degradation of nad5 losing both translation start and stop codons is enriched in the mutant. Our data imply the assembly of mature nad5 mRNA precedes the protection of PPR78.