Control of Volume and Turgor in Stomatal Guard Cells |
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Authors: | Enid AC MacRobbie |
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Institution: | (1) Department of Plant Sciences, University of Cambridge, Downing St., Cambridge, CB2 3EA, UK |
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Abstract: | Water loss from plants is determined by the aperture of stomatal pores in the leaf epidermis, set by the level of vacuolar
accumulation of potassium salt, and hence volume and turgor, of a pair of guard cells. Regulation of ion fluxes across the
tonoplast, the key to regulation of stomatal aperture, can only be studied by tracer flux measurements. There are two transport
systems in the tonoplast. The first is a Ca2+-activated channel, inhibited by phenylarsine oxide (PAO), responsible for the release of vacuolar K+(Rb+) in response to the “drought” hormone, abscisic acid (ABA). This channel is sensitive to pressure, down-regulated at low
turgor and up-regulated at high turgor, providing a system for turgor regulation. ABA induces a transient stimulation of vacuolar
ion efflux, during which the flux tracks the ion content (volume, turgor), suggesting ABA reduces the set-point of a control
system. The second system, which is PAO-insensitive, is responsible for an ion flux from vacuole to cytoplasm associated with
inward water flow following a hypo-osmotic transfer. It is suggested that this involves an aquaporin as sensor, and perhaps
also as responder; deformation of the aquaporin may render it ion-permeable, or, alternatively, the deformed aquaporin may
signal to an associated ion channel, activating it. Treatment with inhibitors of aquaporins, HgCl2 or silver sulfadiazine, produces a large transient increase in ion release from the vacuole, also PAO-insensitive. It is
suggested that this involves the same aquaporin, either rendered directly ion-permeable, or signalling to activate an associated
ion channel. |
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Keywords: | Aquaporin Guard cell Osmoregulation Turgor regulation Tonoplast ion channels |
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