RNA editing in plant mitochondria and plastids converts specific nucleotides from cytidine (C) to uridine (U). These editing events differ among plant species and are relevant to developmental stages or are impacted by environmental conditions. Proteins of the MORF family are essential components of plant editosomes. One of the members, MORF9, is considered the core protein of the editing complex and is involved in the editing of most sites in chloroplasts. In this study, the phenotypes of a T-DNA insertion line with loss of MORF9 and of the genetic complementation line of Arabidopsis were analyzed, and the editing efficiencies of plastid RNAs in roots, rosette leaves, and flowers from the morf9 mutant and the wild-type (WT) control were compared by bulk-cDNA sequencing. The results showed that most of the known MORF9-associated plastid RNA editing events in rosette leaves and flowers were similarly reduced by morf9 mutation, with the exception that the editing rate of the sites ndhB-872 and psbF-65 declined in the leaves and that of ndhB-586 decreased only in the flowers. In the roots, however, the loss of MORF9 had a much lower effect on overall plastid RNA editing, with nine sites showing no significant editing efficiency change, including accD-794, ndhD-383, psbZ-50, ndhF-290, ndhD-878, matK-706, clpP1-559, rpoA-200, and ndhD-674, which were reduced in the other tissues. Furthermore, we found that during plant aging, MORF9 mRNA level, but not the protein level, was downregulated in senescent leaves. On the basis of these observations, we suggest that MORF9-mediated RNA editing is tissue-dependent and the resultant organelle proteomes are pertinent to the specific tissue functions.
RNA editing converts cytidines to uridines in the RNAs transcribed from the chloroplast and mitochondrial genomes in flowering plants. Multiple organellar RNA editing factor (MORF) complex is discovered to be highly associated with C-to-U RNA editing activity of vascular plant editosome. However, mechanism of MORF9 mediating plastid RNA editing controlling plant development and in response to environmental cues remains limited. In this study, we found that loss of MORF9 function impaired PSII efficiency, NDH activity, and carbohydrate production, rapidly promoted nuclear gene expression including sucrose transporter and sugar/energy responsive genes, exhibiting a retard seedling development under sugar starvation condition. When exogenous application of sugar increased transcript and protein level of MORF9 and MORF2 in wild-type, and enhanced the decreasing of matK-706C, accD-794C, ndhD-383C and ndhF-290C RNA editing efficiency in morf9 mutant, and partially recovered altered cell division of root meristem zone, and nuclear gene expression in morf9 mutant. Using gin2, snrk1, morf9 single and double mutants and overexpressing SnRK1 (KIN10) or HXK1 in morf9 mutant background genetically addressed that RNA editing efficiency of ndhD-383C and ndhF-290C sites was declined in the gin2morf9, that of matK-706C, accD-794C, ndhD-383C and ndhF-290C sites was significantly declined in the snrk1morf9, while overexpressing HXK1 or SnRK1 promoted RNA editing rate of matK,accD, ndhD, and ndhF in leaves of morf9 mutant,indicating that HXK1 might require for MORF9 mediating ndhD-383C and ndhF-290C editing, SnRK1 only require for MORF9 mediating ndhF-290C site editing. It suggests that sugar as an energy/sugar signal impairs MORF9 mediating plastid RNA editing affecting plant root development.
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