Abstract
BACKGROUND: Secondary soil salinization adversely affects plant growth in greenhouse in China. Previous studies have suggested that the putative molybdate transporter SlMOT2 may be involved in nitrate stress tolerance in tomatoes. However, the precise regulatory mechanisms remain unclear. RESULTS: Calcium nitrate stress significantly induced the expression of the SlMOT2 gene. In comparison with wild-type (WT) plants, SlMOT2-overexpressing (OE) plants exhibited enhanced tolerance to nitrate stress, as evidenced by lower malondialdehyde (MDA) content, reduced hydrogen peroxide (H₂O₂) accumulation, decline in nitrate accumulation, significantly increased antioxidant enzyme activity, and a higher net photosynthetic rate under nitrate stress conditions, whereas slmot2 knockout mutant plants showed nitrate stress sensitivity. An increasing sulfur level and less nitrate content were also found in overexpression lines of SlMOT2 under calcium nitrate stress. Transcriptomic analysis revealed that nitrate stress induced the upregulation of numerous genes, with the differentially expressed genes (DEGs) in OE plants being significantly enriched in phenylpropanoid biosynthesis, abscisic acid (ABA) synthesis, amino sugar and nucleotide sugar metabolism, and amino acid metabolism in comparison with WT plants. CONCLUSIONS: The SlMOT2 gene confers nitrate stress tolerance in tomato plants, likely through the following molecular mechanisms: (1) enhancing the biosynthesis of antioxidant compounds to improve reactive oxygen species (ROS)-scavenging capacity and maintain photosynthetic efficiency;(2) activating plant hormone signaling transduction pathways to potentiate stress responses; (3) promoting sulfate uptake to rebalance excess nitrogen in planta, thereby establishing a new nitrogen-sulfur homeostasis. These findings establish a theoretical framework for improving nitrate stress resistance during tomato cultivation.