Stomata are microscopic pores on the surface of leaves, each surrounded by a pair of specialized epidermal cells referred to as guard cells. The size of the stomatal pore can be regulated through variations in the guard cells’ turgor pressure. Fine tuning of the stomatal aperture is critical for regulating the exchange of oxygen and carbon dioxide and for controlling transpiration at the interface between plant and environment. Such fine control is achieved through a complex network of signal transduction events triggered by endogenous and environmental stimuli and culminates in the activation and/or inactivation of specific ion channels and transporters localized in the tonoplast and the plasma membrane, which alter the solute balance and consequently the turgor pressure in stomatal guard cells.

Changes in turgor pressure affect the shape and size of guard cells, resulting in closure or opening of the stomatal pore (Hetherington 2001; Schroeder et al. 2001; Nilson and Assmann 2007). For stomatal closure, the guard cell outwardly rectifying potassium channel GORK1 mediates K+ efflux from the guard cells (Hosy et al. 2003). Opening of the voltage-regulated GORK channels is promoted by membrane depolarization resulting from inhibition of proton-extruding adenosine triphosphate hydrolases (H+-ATPases) and activation of anion efflux. Efflux of the anions malate2−, Cl−, and NO3− is mediated by two types of anion channels,“slow”(S-type) and “rapid”(R-type). The slow anion channels are encoded by SLOW ANION CHANNEL-ASSOCIATED 1, which is distantly homologous to genes for dicarboxylate/malic acid transport proteins of microorganisms (Vahisalu et al. 2008); the R-type channel remains to be identified at the molecular level.