Pentatricopeptide repeat (PPR) proteins are crucial for organellar gene expression. To establish a tool for gene expression manipulation in Arabidopsis chloroplasts and genetically inaccessible mitochondria, we engineered designer (dPPR) proteins to specifically inhibit the translation of chloroplast and mitochondrial mRNAs by masking their start codons.Unlike prior methods for targeted downregulation of gene expression, which relied on re-targeting natural PPR proteins to RNA sequences closely related to their original targets, our approach employs a fully synthetic P-type PPR scaffold, programmable to bind any RNA sequence of interest. Here, using dPPR-psbK and dPPR-nad7, we targeted the psbKmRNA in chloroplasts and the nad7 mRNA in mitochondria, respectively. Our results demonstrated that dPPR-psbKeffectively binds and inhibits psbK translation with high specificity, resulting in disrupted PSII supercomplexes and reduced photosynthetic efficiency. Similarly, dPPR-nad7 suppressed nad7 translation, leading to decreased NADH oxidase activity in Complex I and growth retardation. By comparing the phenotypes with tobacco psbK knockouts and bir6-2 mutants, we could exclude any physiologically relevant off-target effects. These findings highlight dPPR proteins as precise tools for targeted translation inhibition, enabling functional studies of organellar genes and offering a novel approach for manipulating mitochondrial gene expression with potential applications across diverse plant species.