ABA signal transduction in guard cells is mediated by phospholipase D.
*Jacob T., *Ritchie S., Assmann, S.M., and Simon Gilroy
Biology Department, 208 Mueller Laboratory, The Pennsylvania State University, University Park,
Pennsylvania 16802
* T.J. and S.R. contributed equally to this work.
Abstract.
In guard cells, the plant hormone abscisic acid (ABA) inhibits stomatal opening and induces stomatal closure through the coordinated
regulation of ion transport. Despite this central role of ABA in regulating stomatal function, the signal transduction events leading to altered
ion fluxes remain incompletely understood. We report that the activity of the enzyme phospholipase D (PLD) transiently increased in guard
cell protoplasts at 2.5 and 25 min after ABA application. Treatment of guard cell protoplasts with phosphatidic acid (PtdOH), one of the
products of PLD activity, led to an inhibition of the activity of the inward K+ channel. PtdOH also induced stomatal closure and inhibited
stomatal opening when added to epidermal peels. Application of 1-butanol (1-buOH), a selective inhibitor of PtdOH production by PLD,
inhibited the increase in PtdOH production elicited by ABA. 1-BuOH treatment also partially prevented ABA-induced stomatal closure and
ABA-induced inhibition of stomatal opening. This inhibitory effect of buOH was enhanced by simultaneous application of nicotinamide, an
inhibitor of cADP ribose action. These results suggest that in the guard cell, ABA activates the enzyme PLD, which leads to the production
of PtdOH. This PtdOH is then involved in triggering subsequent ABA responses of the cell via a pathway operating in parallel to cADP
ribose-mediated events.