SlPPR138-mediated RNA editing of <i>rpoC1</i> is essential for chloroplast development in tomato

Leaf color is a crucial determinant of photosynthetic efficiency and crop yield, but the molecular mechanisms regulating chloroplast development in tomato remain incompletely understood. Here, we identified a novel tomato mutant, <i>gret1</i>, that exhibits yellow cotyledons and young leaves that gradually turn green upon maturation. The <i>gret1</i> mutant displays significantly reduced chlorophyll content and defective chloroplast development at early leaf stages, accompanied by changes in expression of genes involved in photosynthesis and chloroplast biogenesis. Genetic analysis revealed that the <i>gret1</i> phenotype is controlled by a single recessive nuclear gene. Using map-based cloning, we identified <i>SlPPR138</i>, encoding a DYW-type pentatricopeptide repeat (PPR) protein, as the causal gene. A T-to-C point mutation in <i>SlPPR138</i> causes a Cys-to-Arg substitution, which disrupts its function. Both genetic complementation and CRISPR/Cas9 knockout experiments validated that the <i>gret1</i> phenotype is caused by the loss of SlPPR138. Mechanistically, we found that SlPPR138 mediates chloroplast RNA editing, particularly affecting the C-to-U editing efficiency of <i>rpoC1</i>, which encodes a core subunit of plastid-encoded RNA polymerase (PEP) complex. These findings demonstrate SlPPR138 is essential for early chloroplast development through RNA editing, providing new insights into the post-transcriptional regulation of photosynthesis in plants.