Calcium-dependent and calcium-independent events in the initiation of stomatal closure by abscisic acid

Abstract

The signal transduction mechanisms by which abscisic acid (ABA) induces net loss of potassium salts from guard cells and closes stomata are not understood. This paper describes the detailed timecourse of the ABA-induced K + (Rb + ) efflux transient in guard cells of Commelina communis L. and its dependence on external Ca 2+ , and compares the effects of short pulses of ABA with that of continuous ABA. The use of short pulses allows the separation of the two phases of the biphasic response. The results show that stimulation of 86 Rb + efflux, in fact, precedes the reported increase in cytoplasmic Ca 2+ . Furthermore, ABA need not be present on the receptors throughout the full response. Once initiated by a threshold exposure to ABA the response takes over, and the efflux can rise after the removal of ABA. The initial stimulation of efflux requires ABA-occupied receptor sites but is insensitive to external Ca 2+ . The slower component, likely to reflect the release of vacuolar tracer, and with a timecourse similar to the reported changes in cytoplasmic Ca 2+ , does not require the continued presence of ABA, but is accelerated by Ca 2+ . There is also rapid desensitization of the ABA receptors, leaving them unable to respond to reapplication of ABA. The results show that the sequence of events involved in the stomatal closure initiated by ABA is complex, and that only some of the processes initiated are Ca 2+ -dependent. The initial rapid stimulation of K(Rb) efflux is Ca 2+ -independent, and is the fastest response to ABA yet reported. This paper clarifies some of the events involved, but the details of the signal transduction remain to be elucidated.