Nitric Oxide and Plant Ion Channel Control

Abstract

Nitric oxide (NO) has profound effects on the regulation of ion channels in plants. Although direct evidence to date comes exclusively from electrophysiological studies of guard cells, there is good reason to expect similar patterns of action in other plant cell types as well. As in animals, NO appears to act through two distinct mechanisms. One mechanism is mediated via stimulation of guanylate cyclase, which leads to a rise in cyclic ADP-ribose and, in turn, an increase in the efficacy of Ca²⁺ release triggered by Ca²⁺ entry across the plasma membrane. This signal cascade underpins intracellular Ca²⁺ release and the elevation of cytosolic-free [Ca²⁺] by the water-stress hormone abscisic acid and leads to profound changes in K⁺ and Cl⁻ channel activities, to facilitate the ion fluxes for stomatal closure. The second mechanism appears to arise from direct, covalent modification of ion channels by NO, notably of the outward-rectifying K⁺ channel at the guard cell plasma membrane. The physiological significance of this process of S-nitrosylation has yet to be explored in depth, but almost certainly is allied to plant cell responses to pathogen attack and apoptosis. Both processes, and ion transport in guard cells generally, are now sufficiently well-defined for a full description with accurate kinetics and flux equations in which all of the key parameters are constrained by experimental data. Thus, guard cells are now a prime focus for integrative (so-called systems biology) approaches. Applications of integrative analysis have already demonstrated the potential for accurately predicting physiological behaviours and signal interactions with membrane ion transport.