SLAH1, a homologue of the slow type anion channel SLAC1, modulates shoot Cl- accumulation and salt tolerance in Arabidopsis thaliana

Abstract

Salinity tolerance is correlated with shoot chloride (Cl-) exclusion in multiple crops, but the molecular mechanisms of long-distance Cl- transport are poorly defined. Here, we characterize the in planta role of AtSLAH1 (a homologue of the slow type anion channel-associated 1 (SLAC1)). This protein, localized to the plasma membrane of root stelar cells, has its expression reduced by salt or ABA, which are key predictions for a protein involved with loading Cl- into the root xylem. Artificial microRNA knockdown mutants of AtSLAH1 had significantly reduced shoot Cl- accumulation when grown under low Cl-, whereas shoot Cl- increased and the shoot nitrate/chloride ratio decreased following AtSLAH1 constitutive or stelar-specific overexpression when grown in high Cl-. In both sets of overexpression lines a significant reduction in shoot biomass over the null segregants was observed under high Cl- supply, but not low Cl- supply. Further in planta data showed AtSLAH3 overexpression increased the shoot nitrate/chloride ratio, consistent with AtSLAH3 favouring nitrate transport. Heterologous expression of AtSLAH1 in Xenopus laevis oocytes led to no detectible transport, suggesting the need for post-translational modifications for AtSLAH1 to be active. Our in planta data are consistent with AtSLAH1 having a role in controlling root-to-shoot Cl- transport.