GC metabolism during stomatal opening (left) and stomatal closing (right).  Much is unknown about GC carbon metabolism and some processes are inferred.  In essence, stomatal opening is initiated by H⁺ extrusion (1).  Because the cytosolic [H⁺] is low (10^-7–10^-8 M) and weakly buffered (~10 mM·pH^-1), H⁺ extrusion must be supported by new cytosolic H⁺ sources, such as H⁺-Cl^- symport (3 in Fig. 1) or release of H⁺ during A^- accumulation.  In the latter, starch (2) is degraded to hex-P (3), which is exported to the cytosol and, through glycolysis, provides PEP.  Glycolytic oxidation of the aldehyde to the acid releases one H⁺ to the cytosol.  PEP is carboxylated (4) with HCO₃^-, the synthesis of which releases a second H⁺ (5).  Separately, PM hyperpolarization increases the driving force for suc uptake (6), but control mechanisms are unknown.  Some suc possibly is formed from starch degradation (7).  GC symplastic [suc] increase accounts for a variable portion of the osmolyte requirement to open stomata, which is in opposition to the GC apoplastic [suc] increase that results from transpiration.  Stomatal closing is correlated with mal^- efflux (8) or oxidative decarboxylation (9); evidence is against gluconeogenesis.  The fate of suc during stomatal closure is unknown, but it is possibly converted to starch (10).  Compartments are not to scale.