Signalling mechanisms in the regulation of vacuolar ion release in guard cells

Abstract

• Pharmacological agents were used to investigate the possible involvement of actin in signalling chains associated with abscisic acid (ABA)-induced ion release from the guard cell vacuole, a process which is absolutely essential for stomatal closure. • Effects on the ABA-induced transient stimulation of tonoplast efflux were measured, using 86Rb in isolated guard cells of Commelina communis, together with effects on stomatal apertures. • In the response to 10 μm ABA (triggered by Ca2+ influx rather than internal Ca2+ release), jasplakinolide (stabilizing actin filaments) and latrunculin B (depolymerizing actin filaments) had opposite effects. Both closure and the vacuolar efflux transient were inhibited by jasplakinolide but enhanced by latrunculin B. At 10 μm ABA prevention of mitogen-activated protein (MAP) kinase activation by PD98059 partially inhibited closure and reduced the efflux transient. By contrast, latrunculin B inhibited the efflux transient at 0.1 μm ABA (involving internal Ca2+ release rather than Ca2+ influx). • The results suggest that 10 μm ABA activates Ca2+-dependent vacuolar ion efflux via a Ca2+-permeable influx channel which is maintained closed by interaction with F-actin. A MAP kinase is also involved, in a chain similar to that postulated for Ca2+-dependent gene expression in cold acclimation. © The Authors (2007).