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

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 seedlinglethal phenotype. Loss of function of ZmPPR26 abolishes the editing at atpA-1148 site, and decreases the editing at ndhF-62, rp120-308, rp12-2, 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.

Automated summary

ZmPPR26 is essential for the C-to-U RNA editing and chloroplast biogenesis in maize. Loss of function of ZmPPR26 abolishes editing efficiency, leading to a decrease in chloroplast ATP synthase abundance and accumulation of photosynthetic complexes, ultimately resulting in the albino seedling-lethal phenotype.