ABA-Induced Stomatal Closure Involves ALMT4, a Phosphorylation-Dependent Vacuolar Anion Channel of Arabidopsis.

Stomatal pores are formed between a pair of guard cells and allow plant uptake of CO and water evaporation. Their aperture depends on changes in osmolyte concentration of guard cell vacuoles, specifically of K and Mal Efflux of Mal from the vacuole is required for stomatal closure; however, it is not clear how the anion is released. Here, we report the identification of ALMT4 (ALUMINUM ACTIVATED MALATE TRANSPORTER4) as an ion channel that can mediate Mal release from the vacuole and is required for stomatal closure in response to abscisic acid (ABA). Knockout mutants showed impaired stomatal closure in response to the drought stress hormone ABA and increased whole-plant wilting in response to drought and ABA. Electrophysiological data show that ALMT4 can mediate Mal efflux and that the channel activity is dependent on a phosphorylatable C-terminal serine. Dephosphomimetic mutants of ALMT4 S382 showed increased channel activity and Mal efflux. Reconstituting the active channel in mutants impaired growth and stomatal opening. Phosphomimetic mutants were electrically inactive and phenocopied the mutants. Surprisingly, S382 can be phosphorylated by mitogen-activated protein kinases in vitro. In brief, ALMT4 likely mediates Mal efflux during ABA-induced stomatal closure and its activity depends on phosphorylation.