SIGNALING GATES IN ABSCISIC ACID-MEDIATED CONTROL OF GUARD-CELL ION CHANNELS

Multiple signalling pathways and their messengers - entailing changes in cytosolic-free Ca2+ ([Ca2+](i)), pH (pH(i)) and protein phosphoryla tion - underpin K+ and anion channel control during stomatal movements . This redundancy is wholly consistent with the ability of the guard c ells to integrate the wide range of environmental and hormonal stimuli that affect stomatal aperture. Signal redundancy effects a spectrum o f graded responses by linking pathways to gate signal transmission, an d so boosts or mutes the final 'integrated signal' that reaches each i on channel. All evidence supports a role for the ABI1 protein phosphat ase and protein kinase elements in gating K+ channel sensitivity to pH (i) and ABA. Changes in [Ca2+](i), in turn, are demonstrably sensitive to pH(i). Because each of these signal elements modulate and, in turn , are influenced by the activity of different sets of ion channels, th e additional couplings engender a remarkably complex network, layering positive and negative controls with the ion channels that facilitate ion fluxes for stomatal movement.