PPR767 controls mitochondrial RNA editing to regulate growth and drought tolerance in rice

Mitochondria are vital energy-producing organelles that depend on precise RNA processing for function. In this study, Peng et al. identify PPR767, a mitochondria-localized E-type pentatricopeptide repeat (PPR) protein in rice, as a key regulator of plant architecture and drought tolerance. Loss-of-function mutants of PPR767 displayed stunted growth, thinner stems, narrower leaves, and reduced grain yield. Molecular analyses revealed that PPR767 directly binds mitochondrial RNAs and is essential for RNA editing at four sites in three NADH dehydrogenase genes (nad1, nad3, and nad7), all of which encode core subunits of respiratory complex I. In ppr767 mutants, these editing defects impair complex I activity and disrupt mitochondrial structure. PPR767 also interacts with the editing cofactors MORF1 and MORF8, highlighting its role in assembling a functional mitochondrial editosome. As a consequence of complex I dysfunction, ppr767 mutants accumulate excess reactive oxygen species (ROS) and show increased oxidative stress and compromised drought resistance. Transcriptomic analyses indicated significant shifts in the expression of ROS-related and development genes especially in root tissues, suggesting that PPR767 shapes root architecture and stress responses. This study demonstrates how PPR767 integrates mitochondrial RNA editing with energy metabolism and stress resilience, and provides a potential molecular target for breeding rice varieties with improved drought tolerance and robust growth under adverse conditions. (Summary by Muhammad Aamir Khan @MAKNature1998) Plant Physiol. 10.1093/plphys/kiaf187/8126252