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ZmPPR26,一种 DYW 型五肽重复蛋白,是玉米叶绿体中 atpA-1148 处 C 到 U RNA 编辑所必需的。

ZmPPR26, a DYW-type pentatricopeptide repeat protein, is required for C-to-U RNA editing at atpA-1148 in maize chloroplasts.

机构信息

Key Lab of Plant Development and Environment Adaptation Biology, Ministry of Education, School of Life Sciences, Shandong University, Qingdao, China.

出版信息

J Exp Bot. 2021 Jun 22;72(13):4809-4821. doi: 10.1093/jxb/erab185.

Abstract

Pentatricopeptide repeat (PPR) proteins are involved in the C-to-U RNA editing of organellar transcripts. The maize genome contains over 600 PPR proteins and few have been found to function in the C-to-U RNA editing in chloroplasts. Here, we report the function of ZmPPR26 in the C-to-U RNA editing and chloroplast biogenesis in maize. ZmPPR26 encodes a DYW-type PPR protein targeted to chloroplasts. The zmppr26 mutant exhibits albino seedling-lethal phenotype. Loss of function of ZmPPR26 abolishes the editing at atpA-1148 site, and decreases the editing at ndhF-62, rpl20-308, rpl2-2, rpoC2-2774, petB-668, rps8-182, and ndhA-50 sites. Overexpression of ZmPPR26 in zmppr26 restores the editing efficiency and rescues the albino seedling-lethal phenotype. Abolished editing at atpA-1148 causes a Leu to Ser change at AtpA-383 that leads to a reduction in the abundance of chloroplast ATP synthase in zmppr26. The accumulation of photosynthetic complexes are also markedly reduced in zmppr26, providing an explanation for the albino seedling-lethal phenotype. These results indicate that ZmPPR26 is required for the editing at atpA-1148 and is important for editing at the other seven sites in maize chloroplasts. The editing at atpA-1148 is critical for AtpA function, assembly of ATP synthase complex, and chloroplast biogenesis in maize.

摘要

五肽重复(PPR)蛋白参与细胞器转录物的 C 到 U RNA 编辑。玉米基因组包含超过 600 种 PPR 蛋白,其中很少有发现其在叶绿体中的 C 到 U RNA 编辑中发挥作用。在这里,我们报告了ZmPPR26 在玉米中 C 到 U RNA 编辑和叶绿体生物发生中的功能。ZmPPR26 编码一种靶向叶绿体的 DYW 型 PPR 蛋白。ZmPPR26 突变体表现出白化幼苗致死表型。ZmPPR26 功能丧失会导致 atpA-1148 位点的编辑缺失,并降低 ndhF-62、rpl20-308、rpl2-2、rpoC2-2774、petB-668、rps8-182 和 ndhA-50 位点的编辑。ZmPPR26 在 zmppr26 中的过表达恢复了编辑效率并挽救了白化幼苗致死表型。atpA-1148 位点的编辑缺失导致 AtpA-383 处的亮氨酸到丝氨酸的变化,从而导致 zmppr26 中叶绿体 ATP 合酶的丰度降低。Zmppr26 中光合复合物的积累也明显减少,这解释了白化幼苗致死表型的原因。这些结果表明,ZmPPR26 是 atpA-1148 编辑所必需的,并且对玉米叶绿体中其他七个位点的编辑也很重要。atpA-1148 位点的编辑对于 AtpA 功能、ATP 合酶复合物的组装以及玉米叶绿体的生物发生至关重要。

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