The role of Ca2+and ABA in the regulation of stomatal aperture

Abstract

Gaseous exchange at the leaf surface is regulated through changes in stomatal aperture. These changes are brought about by variation in the turgor of the guard cells that surround the stomatal pore and occur in response to a wide range of environmental stimuli, such as CO2level, light intensity and abscisic acid (ABA) concentration. The transduction of some of these stimuli is thought to involve changes in the cytosolic [Ca2+], [Ca2+]i(Mansfield et al., 1990). This idea has originated from the effects of Ca2+buffers, Ca2+-ionophores and Ca2+ channel blockers on stomatal movements (DeSilva et al., 1985a,o; Schwartz, 1985; Inoue and Katoh, 1987; Schwartzet al., 1988; Smith and Willmer, 1988), coupled with analysis of the effects of stimuli such as ABA on 45Ca2+ fluxes into guard cells (MacRobbie, 1989). The changes in guard cell turgor that cause stomatal movements are brought about by changes in K+ and anion fluxes and organic ion synthesis. Stomatal opening requires K+-uptake by the guard cells and K+-uptake channels have been shown to be regulated by [Ca2+] (Schroeder and Hagiwara, 1989). Similarly, changes in [Ca2+] have been shown to regulate the activity of voltage gated anion channels (Keller et al., 1989, Schroeder and Hagiwara, 1989) which could lead to the opening of the channels responsible for the K+efflux associated with stomatal closure (Schroederet al., 1987; Schroeder and Hagiwara, 1989). Thus, changes in [Ca2+]i represent a potential mechanism for the integration of events leading to the inhibition of stomatal opening and the promotion of stomatal closure. However, until recently there has been no direct evidence for the changes in [Ca2+]iimplicit in this model of Ca2+-dependent stomatal closure.