Effects of ABA on 86Rb+ fluxes at plasmalemma and tonoplast of stomatal guard cells

Abstract

Abscisic acid (ABA) induces a transient stimulation of 86Rb+ from isolated guard cells of Commelina communis L. When ABA is added after 30–50 min of wash‐out in the absence of ABA, when tracer is almost entirely vacuolar, its effects on vacuolar release are measured. When ABA is added early in the wash‐out (at 2–4 min), when both cytoplasm and vacuole are labelled, the resulting efflux includes both vacuolar and cytoplasmic contributions. Detailed comparison of rates of efflux in the absence of ABA, and in the presence of ABA added early and late in the wash‐out, allows the effects of ABA on plasmalemma and tonoplast fluxes to be assessed. Three effects of ABA can be distinguished: these are stimulation of the 86Rb+ flux from vacuole to cytoplasm (by twofold to 6.7‐fold); stimulation of the plasmalemma efflux, by up to twofold, a smaller factor than that of the tonoplast effect and variable between experiments; and a doubling of the half‐time for cytoplasmic exchange in ABA, taken to reflect an increase in cytoplasmic ion content as ions flood out of the vacuole. Concentrations of ABA of 0.1–0.2 µM and 1–10 µM are equally effective in the stimulation of plasmalemma efflux, but the effects on tonoplast fluxes are both delayed and reduced at low external concentrations of ABA. It is argued that the delay reflects the need for a threshold internal ABA to be reached before the initiation of vacuolar release, and the reduction reflects the sensitivity of the extent of activation of tonoplast ion channels to concentration of internal ABA. It is likely that the plasmalemma change is mediated by external ABA, and could be the result of the modulation of the stretch‐activated channel suggested previously.