Journal of Experimental Botany, Vol. 52, No.

363,
Plants under Stress Special Issue, pp. 19591967, October 2001

The role of ion channels in light-dependent

stomatal opening

Petra Dietrich1,3, Dale Sanders2 and Rainer Hedrich1

1
Julius-von-Sachs-Institut fur Biowissenschaften, Lehrstuhl fur Molekulare Pflanzenphysiologie
und Biophysik, Julius-von-Sachs-Platz 2, D-97082 Wurzburg, Germany
2
The Plant Laboratory, Biology Department, University of York, PO Box 373, York YO10 5YW, UK

Received 12 April 2001; Accepted 19 June 2001

Abstract the selection pressure of dry and salty soils, or of low

Stomatal opening represents a major determinant of
plant productivity and stress management. Because
plants lose water essentially through open stomata,
volume control of the pore-forming guard cells rep-
resents a key step in the regulation of plant water
status. These sensory cells are able to integrate
various signals such as light, auxin, abscisic acid,
and CO2. Following signal perception, changes in
membrane potential and activity of ion transporters
finally lead to the accumulation of potassium salts
and turgor pressure formation. This review ana-
lyses recent progress in molecular aspects of ion
channel regulation and suggests how these develop-
ments impact on our understanding of light- and
auxin-dependent stomatal action.
Key words: Guard cell, light, auxin, Kq channel, Hq-ATPase,
14-3-3 protein.
Introduction
Stomata optimize the uptake of CO2 and concomitant
loss of water vapour. This dynamic valve is based on
a proper control of the turgor pressure in guard cells
which, in pairs, surround the stomatal pore. During the
past 400 million years of plant evolution the number of
stomata dramatically increased. Phenomena, especially the
step from microphylla to macrophylla about 360 million
years ago, correlated with the drop in atmospheric CO2-
concentration (Beerling et al., 2001). Due to their inability
to leave their habitats, plants developed strategies to
circumvent the limitations in their surroundings. Under
3
To whom correspondence should be addressed. Fax: q49 931 888 6157.
CO2-concentration (high altitudes) a coevolution of dif-
ferent photosynthetic types and stomatal behaviour took
place. C3, C4, and CAM plants are distinguished on the
basis of their carbon metabolism and water-use efficiency.
In addition, there have evolved C3-C4 intermediates and
C3 plants which switch to CAM when subjected to limited
water supply or increased salt concentration. Today,
many crop plants belong to the C3 type. These plants
lose about 600 molecules H2O per fixed CO2 molecule
(Fig. 1), a ratio determined by infrared gas analysis
(Fig. 1A). C3 crops are cultured in more moderate cli-
mates, while C4 and CAM plants, which are character-
ized by respective water-use efficiencies of about 100 and
10 molecules H2O per CO2 fixed, are found in the hot
and dry regions of the earth (Fig. 1B). C4 plants, which
operate a more efficient CO2 assimilation due to very
low photorespiration rates, are able to assimilate similar
carbon quantities as C3 plants with reduced stomatal
aperture and water loss.
CAM plants, which live in the desert, close their sto-
mata during the day and open them at night when the
water vapour gradient is less steep. The control of stomatal
movement in these plant types has puzzled scientists
for decades. Independently of whether they open in the
light or dark, guard cell swelling and stomatal opening
is accompanied by an accumulation of potassium salts
(Fig. 2). While Kq uptake occurs mainly via highly selec-
tive Kq channels, Cl ions enter the cytoplasm probably
via a HquCl symport mechanism. In addition, malate2
is synthesized following starch breakdown. Depending
on the growth conditions and time of the day, stomatal
movement may also rely on sugar accumulation (Talbott
and Zeiger, 1998; Tallman and Zeiger, 1988).

Society for Experimental Biology 2001

1960 Dietrich et al.
As an interface between the photosynthetic cells and
the atmosphere, guard cells are equipped with a CO2
sensor. When the CO2 concentration in the substomatal
cavity drops, for example, when photosynthetic activity
Fig. 1. Gas exchange measurement on a plant leaf. (A) An infrared gas
analyser determines changes in CO2 assimilation and H2O loss. A
cuvette covers the defined leaf area under investigation. (B) Stoma
embedded in the lower epidermis of a Vicia faba leaf. In this C3 species
about 600 molecules H2O (blue) evaporate for one assimilated CO2
molecule (yellow).
Fig. 2. Components of the osmotic motor. Cl and Kq enter the guard
cell cytoplasm and vacuole to drive turgor formation. In addition to Cl
uptake from the medium, malate2 synthesis contributes to anion
accumulation. Following the osmotic gradient, water entry results in
stomatal opening. AthH2, an Arabidopsis water channel expressed in
guard cells, may contribute to water fluxes and is upregulated by blue
light (Kaldenhoff et al., 1995). Figures 1 and 2 are reprinted from the
scientific movie, From Phenomenon to Molecule (R Hedrich and
H Busch, 1998, produced by Institut fur den Wissenschaftlichen Film
IWF gem. GmbH, 1998). Order numbers are: C2014, C7034, C7041 for
part I through III.
is high, stomata open and enable the influx of CO2.
Likewise, at high CO2 concentration in the absence of
photosynthesis, stomata close and prevent water loss. It
is thus tempting to speculate that guard cells sense light
via the internal CO2 concentration. Various studies,
however, demonstrated that guard cells respond to the
blue and red parts of the visible light spectrum (Serrano
et al., 1988; Sharkey and Raschke, 1981). Red light-
mediated stomatal opening is dependent on photosyn-
thetic electron transport in the guard cell chloroplast.
In contrast to red light, low quantum fluxes of blue light
elicit stomatal opening, indicating that red (chlorophyll)
and blue light receptors work together. This review
focuses on the molecular components of the osmotic
motor of guard cells, which in a light-dependent manner
generates and accumulates osmotica to drive stomatal
opening (Fig. 2; Raschke et al., 1988).
Blue light-dependent proton pumping
A prerequisite for channel-mediated Kq-uptake during
stomatal opening is a hyperpolarization of the membrane
negative of the Nernst potential for potassium. This
hyperpolarization can result from proton extrusion via
the Hq-ATPase (Assmann et al., 1985; Blatt, 1988; Lohse
and Hedrich, 1992; Roelfsema et al., 1998), an electro-
enzyme residing in the guard cell plasma membrane at
high density (Becker et al., 1993).
Only recently were the first recordings published of the
membrane potential, together with ion channel activities,
in guard cells of intact plants (Fig. 3; Roelfsema et al.,
Fig. 3. In planta recordings of the guard cell membrane potential.
Cartoon: double-barrelled microelectrodes are introduced into a guard
cell of an intact Vicia faba plant. Darklight transitions elicit changes in
the membrane potential (lower trace) and ion channel activity (not
shown). (Modified after Roelfsema et al., 2001.)

2001). Upon a darklight transition the plasma
membrane hyperpolarizes. When the photosynthetic
capacity was saturated using a beam of red light, addi-
tional red light proved ineffective in modulating the
membrane potential. By contrast, additional blue light
could trigger a negative shift of the membrane potential.
This blue light-dependent activation of the Hq-ATPase
demonstrates that guard cells in intact plants res-
pond qualitatively and in a similar manner to blue
light as isolated guard cell protoplasts (Assmann et al.,
1985; Gotow et al., 1985; Schroeder, 1988; Shimazaki
et al., 1986).
While it can be assumed that in the presence of con-
tinuous blue light the responsible photoreceptors desen-
sitize (Iino et al., 1985; Roelfsema et al., 2001), the nature
of the blue light receptor of guard cells is under debate
(for review, see Assmann and Shimazaki, 1999). Although
the Arabidopsis mutant hy4 (cry1) lacks the blue light-
inhibition of hypocotyl growth, its blue light-dependent
stomatal opening is not affected. CRY1 is therefore
unlikely to function as the blue light receptor of guard
cells (Eckert and Kaldenhoff, 2000; Frechilla et al.,
1999; Lasce`ve et al., 1999). Likewise, loss of function
mutants with respect to the flavin- and pterin-containing
photoreceptor CRY2 or the NPH1 (non-phototropic
hypocotyl 1) protein kinase lacked a blue light-related
stomatal phenotype (Lasce`ve et al., 1999). Instead, the
carotenoid zeaxanthin has been suggested to mediate
blue light-sensitivity in guard cells (Zeiger, 2000). In line
with this hypothesis, the absence of zeaxanthin in the
Arabidopsis mutant npq1 correlated with the lack of
blue light-sensitivity of mutant stomata in epidermal
peels (Frechilla et al., 1999). A detailed infrared gas
analysis (cf. Fig. 1A) on the light-sensitivity of stomata in
various Arabidopsis mutants, however, could demonstrate
that the blue light-dependent stomatal opening in npq1
was comparable to the wild type (Eckert and Kaldenhoff,
2000). Very recently, the NPH1 homologue NPL1 (NPH-
like 1) has been shown to be required for the light
avoidance response of chloroplasts in Arabidopsis leaves
(Kagawa et al., 2001). Therefore, this blue light receptor
or that responsible for the chloroplast accumulation
response in weak light and homologues thereof may
underlie blue light-dependent guard cell processes as well.
Coupling of Hq-ATPase and Kq uptake
channels
Accumulation of potassium during stomatal opening
is thought to be mediated by inward-rectifying Kq
channels which open upon hyperpolarization (Assmann
and Haubrick, 1996; Grabov and Blatt, 1998a; Hedrich
et al., 1998; MacRobbie, 1998; Thiel and Wolf, 1997;
Ward and Schroeder, 1997; Willmer and Fricker, 1996;
Ion channel regulation and stomatal opening 1961
Zimmermann et al., 1999). Apoplastic Kq concentrations
during stomatal opening decrease from about 15 mM
in the dark to 3 mM in the light (Felle et al., 2000;
Szyroki et al., 2001). Together with cytoplasmic Kq con-
centrations rising from about 100 to 400 mM (Raschke,
1979), stomatal opening will result in a negative shift of
the Nernst potential for Kq (EK), from about 60 to
130 mV. Irrespective of these changes in EK, Kq uptake
channels will be gated open with the same voltage-
sensitivity (Blatt, 1992; Bruggemann et al., 1999a). Thus,
only at membrane potentials negative of both the
activation potential of the Kq channel and the EK
accumulation of Kq salts will take place.
In the light, average resting potentials of 112 mV
have been measured in hyperpolarized guard cells of intact
Vicia faba plants (Fig. 3; Roelfsema et al., 2001). In this
hyperpolarized state of the guard cell which accompanies
stomatal opening, the membrane potential lies only
slightly negative of the activation potential of the Kq
uptake channel, a voltage gradient sufficient for Kq
accumulation via inward-rectifying Kq channels (Blatt,
1991; Roelfsema and Prins, 1998; Thiel et al., 1992).
Besides this direct electrical coupling of the Hq-ATPase
and Kq uptake channels, regulatory mechanisms through
pump-driven apoplastic acidification have been shown
to alter the Kq uptake capacity. Impalement studies on
guard cells within epidermal strips and patch-clamp
analysis on protoplasts derived thereof have reported on
the acid activation of Kq uptake channels (Blatt, 1992;
Bruggemann et al., 1999b; Dietrich et al., 1998; Ilan et al.,
1996). Therefore, voltage- and proton-dependent coup-
ling of the Hq-ATPase and Kq uptake channels seem
to represent part of the mechanism underlying stomatal
opening. Apoplastic acidification acts through a change
in the voltage-sensitivity and number of Kq uptake chan-
nels (Blatt, 1992; Dietrich et al., 1998; Hoth et al., 1997a;
Ilan et al., 1996). Assuming one titratable pH-sensitive
site, a pKa value of 5.3 was determined for Kq uptake
channels in Vicia faba (Ilan et al., 1996). This value lies
well within the range of light-induced apoplastic pH
changes in this plant species (Fig. 4). A detailed com-
parison of the guard cell inward rectifier from different
species revealed maximum pH-sensitivities (pKa) at pH
6.2 in Solanum tuberosum and Nicotiana tabacum and
pH 4.8 in Arabidopsis thaliana (Bruggemann et al., 1999b;
Dietrich et al., 1998). Kq uptake into guard cells there-
fore seems to depend on the rate of Hq pumping and
apoplastic pH buffer capacity of the individual species.
The Kq channel-intrinsic pH sensor
Insights into the molecular mechanism of the pH-
dependence were obtained by a mutational analysis of
the Kq uptake channel KST1, which is highly expressed
1962 Dietrich et al.
in guard cells of Solanum tuberosum (Hoth et al., 1997a, b;
Hoth and Hedrich, 1999a, b; Muller-Rober et al., 1995).
Together with KAT1, the guard cell homologue cloned
from Arabidopsis thaliana (Anderson et al., 1992;
Fig. 4. In planta technique non-invasively to monitor changes in ion
concentrations around stomata. Ion-selective microelectrodes are intro-
duced through an open stoma. Changes in Kq, Cl , Ca2q, and Hq can
be followed (Felle et al., 2000). Upon a lightdark transition, the
Hq-concentration of the stomatal apoplast decreases (lower trace), and
vice versa, starting from pH 5.0 in the light-adapted Vicia faba leaf. Note
that the arrow indicates an acidification by 0.5 pH units. pH-recording
with kind permission by Hubert Felle, University of Giessen.
q
Fig. 5. Plant K channel family. (A) Phylogenetic tree of Shaker-like
plant Kq channels (modified after Ache et al., 2000). Five subfamilies
can be distinguished on the basis of their amino acid sequence
homology. (B) Predicted structure of one Kq channel subunit. N- and
C-terminus face the cytoplasmic side of the membrane; S, trans-
membrane segment; P, pore region.
Nakamura et al., 1995), KST1 represents a member of
a large plant Kq channel family (Fig. 5A; for review, see
Hedrich and Dietrich, 1996; Hedrich et al., 1998). The
common structure is characterized by six transmembrane
domains, a pore region between the fifth and sixth
membrane spanning segment, and cytoplasmic N- and
C-termini (Fig. 5B; Becker et al., 1996; Dreyer et al., 1998;
Hoth et al., 1997b; Marten and Hoshi, 1997; Nakamura
et al., 1997; Uozumi et al., 1998). Assembly of four iden-
tical or even different subunits results in a functional
channel protein (Daram et al., 1997; Dreyer et al., 1997;
Ehrhardt et al., 1997; Pilot et al., 2001). Since KST1 and
KAT1 activities very closely resemble the native Kq
inward-rectifying currents from guard cells of Solanum
tuberosum and Arabidopsis thaliana they were assumed to
represent the molecular mechanism of Kq uptake into
guard cells (Fig. 6; Bei and Luan, 1998; Bruggemann
et al., 1999b; Dietrich et al., 1998; Ichida et al., 1997;
Muller-Rober et al., 1995; Pei et al., 1997; Roelfsema and
Prins, 1997). Besides similarities in voltage-dependence,
kinetics and selectivity, the heterologously expressed
Kq channels retained the pH-sensitivity of the functional
Kq channels recorded in their natural environment. To
identify the functional domain responsible for acid acti-
vation in KST1, two histidines, which are exposed to
the extracellular face of the membrane, were mutated
Fig. 6. Electrophysiological recordings in vivo and after heterologous
expression of guard cell channels. Upper graph: Whole-cell recording of
a guard cell protoplast (left) revealing the activation of Kq uptake
channels upon membrane hyperpolarization (right). Lower graph:
Double-electrode voltage-clamp technique applied to a KST1-expressing
Xenopus oocyte (left). Inward Kq currents similar to those observed
in vivo (upper graph) can be resolved (right). (Modified after
Bruggemann et al., 1999b.)

(Hoth et al., 1997a). When both histidines, one in the
linker between S3 and S4 and one in the pore region
(Fig. 5B), were replaced by alanines, the double mutant
lost its pH-dependence. Further mutations within the
fourth transmembrane segment (S4 in Fig. 5B) revealed
the interaction of the pH sensor with this voltage-sensing
domain (Hoth and Hedrich, 1999a). In line with the more
acidic pKa value for the guard cell Kq uptake channel
in Arabidopsis, mutations of the pore histidine in KAT1
did not affect the pH sensitivity (Hoth and Hedrich,
1999a). Therefore, a more complex pH-sensing mech-
anism was postulated to account for acid activation in
KAT1.
In parallel with the external acidification, a rise in
intracellular Hq-concentration was shown to precede
auxin-induced stomatal opening (Gehring et al., 1990;
Irving et al., 1992). Cytosolic acidification in response to
auxin caused the activation of the guard cell Kq inward
rectifier (Blatt and Thiel, 1994; Grabov and Blatt, 1997;
Thiel et al., 1993) as well as KAT1 expressed in oocytes
(Hoshi, 1995). The Kq uptake channel from guard cells
of Arabidopsis thaliana and KAT1 are characterized by
the same pH-dependent activation kinetics with a pKa of
about 6. Thus, the internal pH-sensor was also assumed
to involve histidine residues in the respective Kq channel
protein. A detailed mutagenesis approach with respect to
all cytoplasmic histidines in KAT1 identified a histidine
in the linker between S2 and S3 as part of the acid
activation process (Tang et al., 2000).
Stomatal opening in KAT1 knock out
Arabidopsis
Using the Kq channel inhibitor Ba2q (Schroeder et al.,
1987) attempts have been undertaken to determine the
impact on the guard cell Kq inward rectifier on stomatal
movement (Kelly et al., 1995). However, stomatal open-
ing in Vicia faba could not be prevented by these
methods. After it was shown that KAT1 is expressed in
guard cells of Arabidopsis (Nakamura et al., 1995), a
KAT1 channel mutant with enhanced Csq-sensitivity
was overexpressed in this species (Ichida et al., 1997).
This approch generated a transgenic line with a higher
sensitivity of stomatal opening toward this alkali metal.
The isolation and phenotypical analysis of a KAT
channel knockout mutant revealed, however, that mutant
stomata, deficient in this Kq uptake channel, open in
response to light or low CO2 concentrations and close
in the presence of ABA similarly to wild type (Szyroki
et al., 2001). Thus, KAT1 appears not to be essential for
stomatal movement. In a search for Kq channels which
compensate the KAT1 defect, real-time RT-PCR on
isolated guard cell protoplasts identified additional Kq
channel transcripts (Szyroki et al., 2001). In wild type and
Ion channel regulation and stomatal opening 1963
KAT1 knockout Arabidopsis, the voltage-dependent Kq
channels KAT2 (Pilot et al., 2001) and AKT1 together
with the largely voltage-independent channel AKT2u3 and
Kq channels of unknown voltage-dependence (AtKC1,
AKT5, and AKT6) colocalize in guard cells. Compared
to KAT1 in the wild type, the other Kq channel genes are
expressed at lower levels, leading to a severe decrease of
inward Kq currents in guard cell protoplasts of KAT1
knockout plants. Therefore, it can be concluded that
multiple Kq channels provide for a Kq channel homeo-
stasis. This guarantees a proper function of these sensory
cells at the interface between the plant body and the
environment.
Guard cell signal transduction
While reports accumulate on cytosolic Ca2q- and pH-
changes associated with ABA- and CO2-induced stomatal
closure, the role of these signals for light- and auxin-
stimulated stomatal opening is still unclear (Assmann,
1999; Assmann and Shimazaki, 1999; MacRobbie, 1998).
When Kq currents before and after a light-induced hyper-
polarization were compared in guard cells of intact Vicia
faba plants, a small decrease in inward Kq currents was
observed, while currents mediated by depolarization-
activated Kq channels remained unaltered (Roelfsema
et al., 2001). Since the latter channel type is affected
by cytoplasmic pH-changes too (Blatt, 1992; Ilan et al.,
1994), it might be concluded that light treatment does
not significantly act through changes in cytoplasmic pH
in planta. Inhibition of inward- but not outward-rectifying
Kq channels after light treatment is thus in line with an
increase in Ca2q-concentration during stomatal opening
(Blatt et al., 1990; Luan et al., 1993). Likewise, cyto-
plasmic Ca2q-signals have been proposed to precede
auxin-induced stomatal opening (Irving et al., 1992).
Calcium
Ca2q-permeable channels in the plasma membrane have
been shown to be involved in ABA-induced stomatal
closure (Grabov and Blatt, 1998b, 1999). However,
besides the obvious contribution of vacuoles to guard
cell osmotic relationships, vacuoles might impact signi-
ficantly on signalling processes by virtue of their ability
to store Ca2q. A surprisingly wide array of Ca2q-perme-
able channels is present in the vacuolar membrane.
Voltage-gated Ca2q channels, activated by membrane
hyperpolarization are quite highly selective for Ca2q over
Kq, suggesting a role in physiological Ca2q mobilization
(Allen and Sanders, 1994b). Channel activity is decreased
as a function of luminal pH, and it is therefore note-
worthy that modest alkalinization of guard cell vacuoles
has been reported during stomatal opening (Bowling and
Edwards, 1984).
1964 Dietrich et al.
Cation-selective channels that are activated by cyto-
solic free Ca2q may potentially catalyse a Ca2q-activated
pathway for cation release from the vacuole. These
slowly-activating vacuolar (SV) channels (Hedrich and
Neher, 1987) were first discovered in vacuoles isolated
from barley mesophyll protoplasts (Hedrich et al., 1986),
but have been shown subsequently to be ubiquitously
distributed among plant cell vacuoles (Allen and Sanders,
1997; Hedrich et al., 1988). One attractive model, first
proposed by Ward and Schroeder, envisages that Ca2q
might activate vacuolar Ca2q release through SV
channels, thereby eliciting Ca2q-induced Ca2q release
(Ward and Schroeder, 1994). This would endow the
channel with a role in amplifying Ca2q signals, perhaps as
they initiate at the plasma membrane or through ligand-
gated vacuolar channels. Nevertheless, a critical question
remains concerning whether SV channels are sufficiently
Ca2q permeable to contribute to Ca2q mobilization and
do have sufficient activity at the negative membrane
voltages (Allen et al., 1998; Bewell et al., 1999; Pei et al.,
1999; Potossin et al., 1997; Schulz-Lessdorf and Hedrich,
1995). Therefore, the potential role of SV channels in all
of these responses remains contentious, even among the
authors of this review.
Redox state
Redox agents might also serve to co-ordinate transport
activities at the two membranes. Guard cell Ca2q
channels in the plasma membrane are effectively activ-
ated by H2O2 (Pei et al., 2000), while reducing agents
activate vacuolar SV channels (Carpaneto et al., 1999).
Hydrogen peroxide is also a potent inhibitor of InsP3-
and cADPR-gated Ca2q channels (GD Dickinson and
D Sanders, unpublished observations). Again, the physio-
logical significance of these observations has yet to be
rationalized. It seems possible that the redox state effect-
ively switches the poise of the cell between states in
which extracellular Ca2q is used as a primary supply of
Ca2q for signalling (oxidizing conditions) and states in
which intracellular Ca2q stores are mobilized (reducing
conditions).
InsP3 and cADP ribose
In addition to these voltage-dependent channels, ligand-
gated Ca2q release channels have been identified in
the vacuole. In guard cells, inositol 1,4,5-trisphosphate-
(InsP3-) gated channels can mobilize vacuolar Ca2q
(Allen et al., 1995; Allen and Sanders, 1994a; Gilroy
et al., 1990). Distinct and potent gating of Ca2q channels
by cyclic ADP-ribose (cADPR) has suggested a role for
ryanodine receptor-like channels in Ca2q release from
guard cell vacuoles, and this notion is supported by the
findings that antagonists of cADPR production are inhi-
bitors of stomatal closure in response to ABA (Leckie
et al., 1998). The relative roles of InsP3 and cADPR in
controlling vacuolar mobilization of Ca2q in guard
cells during the stomatal closing response have yet to be
explored.
14-3-3 proteins
14-3-3 proteins, which activate tomato-cell outward
rectifying Kq channels and plasma membrane Hq pumps
in a variety of tissues (Baunsgaard et al., 1998; Booij et al.,
1999) and down-regulate mitochondrial and chloroplast
ATP synthases (Bunney et al., 2001), also markedly
reduce currents through SV channels in mesophyll cells
(van den Wijngaard et al., 2001). For the guard cell
Hq-ATPase from Vicia faba the involvement of 14-3-3
proteins in the blue light-dependent activation of the
pump could be demonstrated (Kinoshita and Shimazaki,
1999). Thereby, the binding of 14-3-3 proteins to the
phosphorylated autoinhibitory C-terminal domain pre-
vents its interaction with the catalytic site leading to a
high-activity state of the Hq-ATPase. In addition to
blue light, hyperactivation of the plasma membrane
Hq-ATPase and stomatal opening are also observed
after treatment with the fungal elicitor fusicoccin (Blatt,
1988). In contrast to blue light-stimulation, fusicoccin
seems to stabilize the complex between Hq-ATPase and
14-3-3-protein even in the absence of a phosphorylated
residue (Baunsgaard et al., 1998; Fullone et al., 1998).
Fusicoccin has been shown to inhibit guard cell outward
Kq currents (Blatt and Clint, 1989), but a mechanism
involving down-regulation via dissociation of 14-3-3
proteins has not yet been analysed. Therefore, details of
any co-ordinating role for 14-3-3 proteins have yet to be
established. Only recently, the guard cell Kq outward
rectifier, GORK, has been cloned (Ache et al., 2000)
enabling the analysis of how 14-3-3 proteins are involved
in guard cell ion channel regulation and stress
management.
Acknowledgement
RH gratefully acknowledges funding through the DFG
(SFB 251).
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