Abstract

Experiments are described which attempted to clarify the reasons for differences in stomatal opening on adaxial and abaxial epidemics. Previous studies had suggested that endogenous auxin levels might be responsible. It was found that adaxial stomata were more sensitive than abaxial stomata to externally supplied abscisic acid (ABA). It is suggested that differing endogenous concentrations of calcium ions in the upper and lower epidermes may contribute to the observed differences in sensitivity to ABA. It is further suggested that studies of stomata on isolated epidermis may represent a useful model system for examining the role of cell or tissue sensitivity in determining the responses to ABA and other hormones. Data are presented which lend support to the suggestion that calcium ions play an important part. Treatment with lanthanum ions, which block calcium channels in cell membranes, had little effect on abaxial stomata, but caused the apertures of adaxial stomata to increase considerably. The chelating agent EGTA eliminated the differential behaviour of adaxial and abaxial stomata, which clearly suggests that calcium ions have a dominant role. Experiments in which EGTA and fusicoccin were presented separately and in combination indicated that their effects were independent and additive. It is suggested that they operate at different locations, or on different processes in the guard cells.

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