COP1 proteins integrate light signaling to fruit plastid development via the HY5-GLK2 module in tomato

Light signaling regulates plant development, yet how it differentially controls plastid development across organs remains unclear. Here, we show that two tomato COP1 proteins restrict plastid development in fruits but not in leaves. With CRISPR-Cas9 mutants, we demonstrate that SlCOP1s repress photomorphogenesis by destabilizing SlHY5 and controlling large-scale light-responsive transcription in seedlings. In fruits, SlCOP1s suppress chloroplast development and chlorophyll accumulation by inhibiting SlHY5-dependent activation of GLK2, a key regulator of plastid biogenesis. SlHY5 directly binds the GLK2 promoter and activates its expression in fruits, but not in leaves, highlighting tissue-specific deployment of the SlCOP1-SlHY5 module. This pathway is distinct from CUL4-DDB1-DET1-mediated regulation of GLK stability, indicating multilayered control of GLK2. Enhanced plastid development in Slcop1 double mutants is associated with increased carotenoid accumulation in fruit. Together, these findings uncover a SlCOP1-SlHY5-GLK2 module that links light signaling to fruit plastid development and illustrate how conserved pathways are rewired to control organelle development in a tissue-dependent manner.