Figure 4 |. Guard cell signal transduction and stomatal responses to environmental stimuli.

a | Schematic model of abscisic acid (ABA) signal transduction in guard cells. ABA transporters mediate ABA import or export from guard cells. In the presence of ABA, the key regulator SNF1-RELATED PROTEIN KINASE 2.6/OPEN STOMATA 1 (SnRK2.6/OST1) phosphorylates and activates SLOW ANION CHANNEL-ASSOCIATED 1 (SLAC1), ALUMINUM-ACTIVATED MALATE TRANSPORTER 12/QUICK-ACTIVATING ANION CHANNEL 1 (ALMT12/QUAC1), and RESPIRATORY BURST OXIDASE HOMOLOGs (RBOHs). Activation of the S-type anion channel SLAC1 and the R-type anion channel ALMT12/QUAC1 leads to long-term plasma membrane depolarization, which causes K⁺ efflux through the voltage-dependent K⁺_out channel GUARD CELL OUTWARD RECTIFYING K⁺ CHANNEL (GORK). Activated RBOH NADPH oxidases produce ROS that mediate HYDROGEN-PEROXIDE-INDUCED Ca²⁺ INCREASES 1 (HPCA1) sensor-dependent activation of Ca²⁺-permeable I_Ca channels, resulting in the elevation of the cytosolic Ca²⁺ concentration ([Ca²⁺]_cyt). Elevated [Ca²⁺]_cyt activates Ca²⁺-sensor proteins including Ca²⁺-DEPENDENT PROTEIN KINASEs (CPKs) that phosphorylate and activate SLAC1. The (pseudo-)kinase GUARD CELL HYDROGEN PEROXIDE-RESISTANT 1 (GHR1) mediates the activation of I_Ca and SLAC1 channels through an unknown mechanism, possibly as scaffolding protein. SnRK2.6/OST1 inhibits the K⁺_in channel K⁺ CHANNEL IN ARABIDOPSIS THALIANA 1 (KAT1), that mediates K⁺ uptake, by direct phosphorylation. In addition, SnRK2.6/OST1 causes a long-term decrease of KAT1 expression by inhibition of ABA-RESPONSIVE KINASE SUBSTRATE (AKS) transcription factors. ABA also inhibits H⁺-ATPase activity through SnRK2.6/OST1, but the detailed mechanism is unknown. Dashed lines indicate steps that are inhibited in the presence of ABA. Note that only guard cell ABA signaling regulating ion transport across the plasma membrane is depicted in this figure. b | In addition to drought stress, several other environmental stimuli can be perceived by guard cells and affect stomatal aperture though sophisticated signaling crosstalk and integration.