Plasma membrane ion channel regulation during abscisic acid-induced closing of stomata

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Abstract
The plant growth regulator abscisic acid triggers closing of stomata in the leaf epidermis in response to water stress. Recent tracer flux studies, patch-clamp studies, fluorometric Ca 2+ measurements and microelectrode experiments have provided insight into primary transduction mechanisms by which abscisic acid causes stomatal closing. Data show that abscisic acid activates non-selective Ca 2+ permeable ion channels in the plasma membrane of guard cells. The resulting elevation in the free Ca 2+ concentration in the cytosol of guard cells, and the resulting membrane depolarization as well as other unidentified Ca 2+ independent mechanisms are suggested to contribute to activation of voltage- and second messenger-dependent anion channels and outward rectifying K + channels. Recent data suggest the involvement of two types of anion channels in the regulation of stomatal movements, which provide highly distinct mechanisms for anion efflux and depolarization. A novely characterized ‘S-type’ anion channel is likely to provide a key mechanism for long-term depolarization and sustained anion efflux during closing of stomata. Patch-clamp studies have revealed the presence of a network of K + , anion and non-selective Ca 2+ -permeable channels in the plasma membrane of a higher plant cell. The integrated control of these guard cell ion channels by abscisic acid can provide control over K + and anion efflux required for stomatal closing.