KIN7 kinase regulates the vacuolar TPK1 K+ channel during stomatal closure

Stomata are leaf pores that regulate CO 2 uptake and evapotranspirational water loss. By controlling CO 2 uptake, stomata impact on photosynthesis and dry matter accumulation. The regulation of evapotranspiration is equally important because it impacts on nutrient accumulation and leaf cooling and enables the plant to limit water loss during drought [1]. Our work centers on stomatal closure [2–6]. This involves loss of potassium from the guard cell by a two-step process. Salt is released across the plasma membrane via anion channels such as SLAC1 [7–9] and depolarization-activated channels such as GORK [10, 11], with the net result that cations and anions exit guard cells. However, this critically depends on K + release from the vacuole; with ∼160 and 100 mM K + in cytoplasm and vacuole of open guard cells [12], vacuolar K + efflux is driven by the negative tonoplast potential, and this expels K + from the vacuole via tonoplast K + channels like TPK1. In all, guard cell salt release leads to a loss of turgor that brings about stomatal closure. First, we show that the TPK1 vacuolar K + channel is important for abscisic acid (ABA)- and CO 2-mediated stomatal closure. Second, we reveal that, during ABA- and CO 2-mediated closure, TPK1 is phosphorylated and activated by the KIN7 receptor-like protein kinase (RLK), which co-expresses in the tonoplast and plasma membrane. The net result is K + release from the vacuole. Taken together, our work reveals new components involved in guard cell signaling and describes a new mechanism potentially involved in fine-tuning ABA- and CO 2-induced stomatal closure. Stomatal closure critically depends on K + release from the guard cell vacuole. Isner et al. show that the TPK1 vacuolar K + channel is important for ABA- and CO 2-mediated stomatal closure and that channel activation involves TPK1 phosphorylation by the KIN7 receptor-like protein kinase, which co-expresses in the tonoplast and plasma membrane.