Soil salinization poses a serious threat to plant development and represents a major obstacle to the sustainable production of crops worldwide. Melatonin (MT) contributes prominently to plant tolerance against abiotic environments. However, the molecular basis of transcriptional regulation underlying melatonin accumulation in tomato under saline–alkali stress is still largely unknown. Herein, we identify SlNAC2, a NAC transcription factor in tomato induced by saline–alkali stress, which suppresses the key melatonin biosynthetic genes SlCOMT2 and SlSNAT, while activating SlCV, a gene linked to reactive oxygen species (ROS) accumulation and programmed cell death. These regulatory effects reduce MT levels and promote excessive ROS production, ultimately altering the plant’s tolerance to saline–alkali stress. Silencing of SlNAC2 through the RNA interference method significantly improves saline–alkali tolerance in tomato, while its constitutive overexpression shows increased susceptibility to saline–alkali stress. Further evidence reveals that under saline–alkali conditions, SlNAC2 directly targets cis-elements of SlCOMT2 and SlSNAT promoters, suppressing their transcription and consequently reducing melatonin levels, whereas simultaneously binding to the SlCV promoter to activate its expression, ultimately leading to ROS accumulation. Moreover, comprehensive protein interaction analyses confirmed that SlNAC2 physically associates with SlDREB2, a DREB-type transcription factor involved in salt stress response. Through its interaction with SlNAC2, SlDREB2 partially attenuates its repression of SlCOMT2 and SlSNAT, thereby increasing melatonin accumulation and ROS scavenging, ultimately enhancing tomato’s resilience to saline–alkali stress conditions. Collectively, our findings reveal a SlNAC2–SlDREB2 regulatory module that finely tunes melatonin synthesis and ROS levels to regulate tomato’s response to saline–alkali stress, providing new strategies for developing stress-resilient tomato varieties.

Full text PDF download