Role of calcium in the modulation of Vicia guard cell potassium channels by abscisic acid: A patch-clamp study

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Abstract
There is evidence for a role of increased cytoplasmic Ca2+ in the stomatal closure induced by abscisic acid (ABA), but two points of controversy remain the subject of vigorous debate—the universality of Ca2+ as a component of the signaling chain, and the source of the increased Ca2+, whether influx across the plasmalemma, or release from internal stores. We have addressed these questions by patch-clamp studies on guard cell protoplasts of Vicia faba, assessing the effects of ABA in the presence and absence of external Ca2+, and of internal Ca2+ buffers to control levels of cytoplasmic Ca2+. We show that ABA-induced reduction of the K+ inward rectifier can occur in the absence of external Ca2+, but is abolished when Ca2+ buffers are present inside the cell. Thus, some minimum level of cytoplasmic Ca2+ is a necessary component of the signaling chain by which ABA decreases the K+ inward rectifier in stomatal guard cells, thus preventing stomatal opening. Release of Ca2+ from internal stores is capable of mediating the response, in the absence of any Ca2+ influx from the extracellular medium. The work also shows that enhancement of the K+ outward rectifier by ABA is Ca2+ independent, and that other signaling mechanisms must be involved. A role for internal pH, as suggested by H.R. Irving, C.A. Gehring and R.W. Parish (Proc. Natl. Acad. Sci. USA 89:1790–1794, 1990) and M.R. Blatt (J. Gen. Physiol. 99:615–644, 1992), is an attractive working hypothesis.