SUGGESTED INVOLVEMENT OF CALCIUM AND CALMODULIN IN THE RESPONSES OF STOMATA TO ABSCISIC ACID

Abstract

S ummary A requirement for calcium during the inhibition of stomatal opening by abscisic acid (ABA) was reported in a previous study, and evidence is now presented which gives further indications of the part played by calcium. Calcium‐channel blockers (lanthanum, verapamil and nifedipine) reduced the ability of stomata to respond to ABA. A calcium ionophore (A 23187) reduced stomatal opening, presumably because it mimicked the effect of ABA in increasing permeability of the plasma membrane to calcium. In the presence of three calmodulin antagonists, the inhibitory effect of ABA was much reduced. The synthetic auxin naphth‐l‐ylacetic acid (NAA) prevented stomatal opening, but this action did not appear to be dependent on calcium ions. It is suggested that the action of ABA on guard cells requires a free passage of calcium ions into the cytosol. They may act as second messengers, interacting with calmodulin to produce the overt cellular responses to ABA. Although the data presented apply only to stomata, these experiments may have provided insight into the basic mechanism by which ABA acts on cellular processes. It is suggested that some reported effects of Ca 2+ on the action of other plant growth substances could have resulted from complex interactions involving endogenous ABA.