Key message <p><i>SlSNAT1</i>-dependent melatonin synthesis enhances tomato cold tolerance by promoting <i>SlNCED1</i>-mediated ABA accumulation, thereby strengthening antioxidant capacity, maintaining photosynthesis, and reducing ROS-induced membrane damage under cold stress.</p> Abstract <p>Cold stress limits greenhouse tomato growth by suppressing photosynthesis, promoting reactive oxygen species (ROS) accumulation, and disrupting membrane integrity, which ultimately reduces yield. Melatonin (MT) enhances plant stress tolerance, but its role in regulating cold adaptation in tomato remains unclear. Here, we used CRISPR/Cas9-generated <i>SlSNAT1</i> mutants and VIGS-mediated <i>SlNCED1</i>-silenced plants to test how MT influences abscisic acid (ABA) biosynthesis and cold tolerance. The <i>SlSNAT1</i> mutation markedly reduced endogenous MT, decreased the expression of ABA biosynthetic genes (<i>SlNCED1/2</i>), and increased the expression of ABA catabolic genes (<i>SlCYP707A1/2</i>), thereby weakening cold-induced ABA accumulation. Accordingly, the mutants showed higher membrane permeability and ROS levels, together with lower photosynthetic efficiency and reduced antioxidant enzyme activity under cold stress. <i>SlNCED1</i> silencing further reduced ABA accumulation and antioxidant capacity. By contrast, exogenous MT partly restored ABA content, antioxidant enzyme activity, and photosynthetic performance, thereby alleviating cold injury. Correlation analysis showed that ABA content was positively associated with antioxidant activity, photosynthetic traits, and osmotic regulators, but negatively associated with ROS levels and membrane damage. MT synthesis mediated by <i>SlSNAT1</i> promotes ABA accumulation, at least in part, by enhancing <i>SlNCED1</i> expression. These findings clarify a mechanism underlying MT–ABA cross talk during cold stress and suggest a potential strategy to enhance cold tolerance in greenhouse tomato.</p>