Figure 9.

Schematic model for environmental factor-induced stomatal closure (A) and summary of the stomatal responses of mutants characterized in this study (B). A, The emerging model suggests that in the case of O₃, all components of the ABA signalosome are required to trigger stomatal closure. For reduced air humidity, we show that the ABA signalosome plays an important role; however, the presence of a parallel, ABA-independent pathway (marked as 1) was suggested by Assmann et al. (2000) and Xie et al. (2006). Darkness-induced stomatal closure is mediated by increased intercellular CO₂ concentration that activates anion channels and by inactivation of H⁺-ATPase (Roelfsema et al., 2002; Shimazaki et al., 2007). CO₂-induced stomatal closure involves the activation of carbonic acid anhydrases that convert CO₂ to HCO₃⁻. The results presented in this study suggest that CO₂-induced stomatal closure and HCO₃⁻-induced activation of S-type anion channels are partly controlled by the ABA signalosome. Question marks highlight that the nature of signal perception at the plasma membrane and signal transduction in the cytosol leading to the activation of the ABA signalosome remain to be addressed. B, Summary of stomatal responses to closure-inducing stimuli in the studied mutants. Mutants are presented in the order of phenotypic severity. H and D indicate air humidity and darkness, respectively. + indicates that either initial change in g_st or curve fitting was different from the wild type, and ++ indicates that initial change in g_st and curve fitting were both different from the wild type. The absence of a symbol indicates wild-type-like stomatal closure. Mutants that showed wild-type-like stomatal responses to all stimuli (148, cpk21, cyp707a1, and cyp707a3) are not listed here. [See online article for color version of this figure.]