Abstract

Aluminium (Al) toxicity in acidic soils severely inhibits root growth and plant productivity. While organic acid exudation (malate, citrate and oxalate) is a key Al-tolerance mechanism, the transporters and regulatory networks in tomato ( Solanum lycopersicum ) remain poorly characterised. Here, we identified the slow anion channel SlSLAH1 as a plasma membrane-localised malate transporter essential for Al tolerance. Under Al stress, the transcription factor SlSTOP1 and its enhancer SlSZP1 accumulated and formed a complex that directly bound to the SlSLAH1 promoter, activating its expression and enhancing malate exudation from roots. Concurrently, Al stress induced SlSLAH2 expression independently of SlSTOP1. SlSLAH2 interacted with SlSLAH1 to form a heteromeric complex at the plasma membrane, which synergistically facilitated malate exudation. Genetic analyses confirmed that knockout mutants of Slslah1 or Slslah2 exhibited reduced malate exudation and increased Al sensitivity, while SlSLAH1 overexpression lines showed enhanced Al tolerance. Our study unveils a regulatory module where the SlSTOP1-SlSZP1 complex and SlSLAH1-SlSLAH2 heteromeric complex jointly orchestrate malate exudation to confer Al tolerance in tomato, providing mechanistic insights into aluminium detoxification and developing aluminium-tolerant germplasm.