Filomena Vanessa Loiacono, Wolfram Thiele, Mark Aurel Schöttler, Michael Tillich, Ralph Bock
In chloroplasts and plant mitochondria, specific cytidines in mRNAs are posttranscriptionally converted to uridines by RNA editing. Editing sites are recognized by nucleus-encoded RNA-binding proteins of the pentatricopeptide repeat (PPR) family, which bind upstream of the editing site in a sequence-specific manner and direct the editing activity to the target position. Editing sites have been lost many times during evolution by C-to-T mutations. Loss of an editing site is thought to be accompanied by loss or degeneration of its cognate PPR protein. Consequently, foreign editing sites are usually not recognized when introduced into species lacking the site. Previously, the spinach () -26 editing site was introduced into the tobacco () plastid genome. Tobacco lacks the -26 site and cannot edit it. Expression of the "unedited" PsbF protein resulted in impaired PSII function. In Arabidopsis (), the PPR protein LPA66 is required for editing at -26. Here, we show that introduction of the Arabidopsis LPA66 reconstitutes editing of the spinach -26 site in tobacco and restores a wild-type-like phenotype. Our findings define the minimum requirements for establishing new RNA editing sites and suggest that the evolutionary dynamics of editing patterns is largely explained by coevolution of editing sites and PPR proteins.
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