GC membrane-transport processes during stomatal opening (left) and stomatal closing (right).  Transporters in a conducting state are green; in a nonconducting state, red; conducting state not specified, blue.  Note, as indicated, that one icon may represent several transporters having different properties.  The traffic-control icon by a transporter indicates inhibition (red, upper) or activation (green, lower); effectors act directly and indirectly.  The roles of some transporters are not assigned with certainty.  In essence, stomatal opening is initiated by H⁺ extrusion (1), which hyperpolarizes the PM and acidifies the apoplast.  These effects increase the driving force for K⁺ uptake and activate the voltage-regulated K⁺-in channel (2).  Cl^- (3) and suc (4) may also be taken up.  H⁺ pumping into the vacuole (5, 6) provides for K⁺ antiport (7) and Cl^- uptake (8).  GC solute increase leads to H₂O uptake and therefore an increase in GC volume and aperture size.  Stomatal closing is initiated by activation of the A^- channel (9), which depolarizes the PM.  This effect increases the driving force for K⁺ efflux and activates the voltage-regulated K⁺-out channel (10).  Several channels (11) provide for solute release from the vacuole.  Internal and external ABA receptors (12) cause the release of Ca²⁺ through cellular messengers (e.g., IP₃); ABA also causes Ca²⁺ influx (13).  ABA also induces stomatal closure by Ca²⁺-independent means.  Compartments are not to scale.