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Article|28 Jul 2025|OPEN
SlPPR138-mediated RNA editing of rpoC1 is essential for chloroplast development in tomato
Yichen Liu1 , Chengwen Li1 , Xiuyang Si1 , Tao Zou1 , Ye Li2 , Changtian Pan1,3 , , Gang Lu,1,4 ,
1Department of Horticulture, College of Agriculture and Biotechnology, Zhejiang University, Hangzhou 310058, China
2Department of Agronomy, HeiLongJiang Agricultural Engineering Vocational College, Harbin 150088, China
3Zhejiang Key Laboratory of Horticultural Crop Quality Improvement, Zhejiang University, Hangzhou 310058, China
4Key Laboratory of Horticultural Plant Growth, Development and Quality Improvement, Ministry of Agricultural, Zhejiang University, Hangzhou 310058, China
*Corresponding author. E-mail: pct@zju.edu.cn,glu@zju.edu.cn

Horticulture Research 12,
Article number: uhaf194 (2025)
doi: https://doi.org/10.1093/hr/uhaf194
Views: 183

Received: 17 Apr 2025
Accepted: 18 Jul 2025
Published online: 28 Jul 2025

Abstract

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, gret1, that exhibits yellow cotyledons and young leaves that gradually turn green upon maturation. The gret1 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 gret1 phenotype is controlled by a single recessive nuclear gene. Using map-based cloning, we identified SlPPR138, encoding a DYW-type pentatricopeptide repeat (PPR) protein, as the causal gene. A T-to-C point mutation in SlPPR138 causes a Cys-to-Arg substitution, which disrupts its function. Both genetic complementation and CRISPR/Cas9 knockout experiments validated that the gret1 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 rpoC1, 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.