The SlLRR‐RLK94‐SlPti1a Module Enhances Salt Tolerance by Modulating Reactive Oxygen Species and Hormone Homoeostasis in Tomato

Tomato ( Solanum lycopersicum ) is a globally cultivated crop of high economic and nutritional importance, yet its growth and productivity are severely threatened by soil salinization. Although leucine‐rich repeat receptor‑like kinases (LRR‐RLKs) are key environmental sensors, the mechanisms governing tomato salt tolerance remain elusive. Here, we demonstrate that the SlLRR‑RLK94 and its downstream interacting protein, the receptor‑like cytoplasmic kinase SlPti1a, form a functional plasma membrane complex that positively regulates salt tolerance in tomato. CRISPR/Cas9‑mediated knockout of SlLRR‑RLK94 or VIGS‑mediated silencing of SlPti1a markedly reduced salt tolerance, resulting in severe leaf chlorosis and restricted root growth under salinity. Disruption of this module severely compromised physiological defence systems, leading to excessive reactive oxygen species accumulation, altered antioxidant enzyme activities, and an elevated Na + /K + ratio caused by uncontrolled Na + buildup. Transcriptomic analysis revealed that loss of SlLRR‑RLK94 extensively reprogrammed metabolic networks under salt stress, impairing photosystem homoeostasis and suppressing the diterpenoid biosynthesis pathway. This transcriptional reprogramming led to an endogenous hormonal imbalance characterised by gibberellin deficiency and abscisic acid accumulation. Collectively, our findings elucidate the molecular mechanisms by which the SlLRR‑RLK94‑SlPti1a module coordinates ionic, oxidative, and hormonal homoeostasis, providing promising genetic targets for breeding salt‑tolerant tomato cultivars.