CmGT9 represses salt tolerance in grafted melon via CmRAP2.6L coordinating ion and redox homeostasis.

Salt stress severely restricts melon (Cucumis melo L.) production, and grafting is widely used to improve salt tolerance; however, the underlying regulatory mechanisms remain unclear. In this study, we identified the trihelix transcription factor CmGT9 as a key negative regulator of salt tolerance in grafted melon using contrasting rootstock combinations. Root-specific manipulation of CmGT9 demonstrated that it suppressed salt tolerance by impairing Na⁺/K⁺ homeostasis. Integrated RNA-seq and DAP-seq analyses identified ion transporter genes CmNHX6, CmKUP11, and CmKUP3, and the ERF transcription factor gene CmRAP2.6 L as direct CmGT9 targets, and CmGT9 bound to their promoters to repress transcription. CmRAP2.6 L functioned downstream as a positive regulator of antioxidant defense; its activation enhanced ROS-scavenging capacity, while loss of function reduced antioxidant enzyme activity and antioxidant metabolite accumulation. Mechanistically, CmRAP2.6 L directly activated antioxidant genes (CmPOD1/CmPOD2 and CmGSTU7-1/CmGSTU8) via GCC-box (GCCGCC) recognition. Collectively, we define a CmGT9-CmRAP2.6 L transcriptional cascade that integrates ion homeostasis with antioxidant defense to regulate salt tolerance, providing potential targets for improving melon rootstock performance.