The DYW domain of RARE1 plays an indispensable role in regulating accD-C794 RNA editing in Arabidopsis thaliana
作者全名:"Liu, Dan; Li, Zi-Ang; Li, Yi; Molloy, David P.; Huang, Chao"
作者地址:"[Liu, Dan; Li, Zi-Ang; Li, Yi; Huang, Chao] Hunan Agr Univ, Coll Biosci & Biotechnol, Changsha 410128, Peoples R China; [Molloy, David P.] Chongqing Med Univ, Basic Med Coll, Dept Biochem & Mol Biol, Chongqing 400016, Peoples R China; [Molloy, David P.] Chongqing Med Univ, Basic Med Coll, Ctr Mol Med & Canc Res, Chongqing 400016, Peoples R China"
通信作者:"Huang, C (通讯作者),Hunan Agr Univ, Coll Biosci & Biotechnol, Changsha 410128, Peoples R China.; Molloy, DP (通讯作者),Chongqing Med Univ, Basic Med Coll, Dept Biochem & Mol Biol, Chongqing 400016, Peoples R China."
来源:PLANT SCIENCE
ESI学科分类:PLANT & ANIMAL SCIENCE
WOS号:WOS:001032591500001
JCR分区:Q1
影响因子:4.2
年份:2023
卷号:334
期号:
开始页:
结束页:
文献类型:Article
关键词:Arabidopsis; Chloroplast RNA editing; RARE1; AtECB2; accD-C794
摘要:"The Arabidopsis pentatricopeptide repeat (PPR) proteins, required for accD RNA editing 1 (RARE1) and early chloroplast biogenesis 2 (AtECB2), each contain a DYW domain deemed essential for cytosine deamination at the accD-C794 RNA editing site in chloroplasts. Complementation assays using the rare1 mutant investigate the correlation between these PPRs and their respective DYW domain functions in RNA editing of accD-C794. The results demonstrate that the coding sequence of AtECB2 cannot replace that of RARE1. Moreover, rare1 mutants complemented with DYW-deleted RARE1 failed to recover the RNA editing of accD-C794 even in the presence of the highly similar DYW domain of the AtECB2 protein. These findings indicate that RARE1 and AtECB2 possess divergent roles in RNA editing, with specificity for accD-C794 directly attributable to DYW domain within RARE1. Structural modeling data suggest this functioning pertains to a local & alpha;-helical motif that residues slightly N-terminal to the consensus glutamate and CXXCH motif in the DYW domain for cytidine deamination during C -to-U editing by RARE1 that is absent within AtECB2."
基金机构:National Natural Science Foundation of China [31900387]; Natural Science Foundation of Hunan Province [2020JJ4037]; Research Foundation of Education Bureau of Hunan Province [2022B112]; Chinese Government Ministry of Scienceand Technology [G2021035005L]
基金资助正文:"This work was supported by the National Natural Science Foundation of China (31900387) , Natural Science Foundation of Hunan Province (2020JJ4037) , the Research Foundation of Education Bureau of Hunan Province (2022B112) and The Chinese Government Ministry of Scienceand Technology (G2021035005L; DM) ."