ABA Regulation of Stomatal Movement - Abscisic Acid: Metabolism, Transport and Signaling - page 292

family. The main plasma membrane K + channels in Arabidopsis guard cells are
mainly from shaker-type K + channel family, and the functions of other channel
families as K + channels in guard cells are less studied. Shaker-type K + channel
family is composed of nine members in Arabidopsis . They share protein struc-
tural similarities, including six transmembrane (TM) domains, a voltage sensor
located in the fourth TM domain, and a P loop between TM five and six. Shaker
channel members can form homo- or heterotetramers. In Arabidopsis guard cells,
the expression of six shaker-type K + channels, including KAT1 , KAT2 , AKT1 ,
AKT2 , GORK, and KC1 , can be detected. GORK is the main outward-rectifying
K + channels, which is activated by the depolarization of the plasma membrane
of guard cells. The T-DNA insertional knockout mutation of GORK abolishes
outward K + channel currents of guard cells completely and impairs dark- and
ABA-induced stomatal closure (Hosy et al. 2003 ). In ABA signaling network, out-
ward anion channels are first activated by upstream kinases as described above,
the efflux of anion through anion channels results in a depolarization of guard
cell plasma membrane, and consequently activate GORK. For stomata opening,
K + influx through inward K + channels is required, and the inward K + channels
in Arabidopsis guard cells can be activated by hyperpolarization voltage. KAT1,
KAT2, AKT1, AKT2, and KC1 are the five proteins forming inward-rectifying
K + channels in Arabidopsis guard cells (Szyroki et al. 2001 ). The five inward-
rectifying K + channel proteins can form homotetramers alone or heterotetramers.
KC1 does not form functional K + channels alone, but can integrate into inward
K + channels as one of the four subunits and function as an inhibitory regulating
subunit. KAT1 is the first inward-rectifying K + channels identified in plant, and
also the main inward-rectifying K + channels in guard cells because the expres-
sion level of KAT1 is much higher than other four members, and the disrup-
tion of KAT1 leads to more than 50 % reduction of inward K + channel activity
in Arabidopsis guard cells (Szyroki et al. 2001 ). Dominant negative repressive
mutants of KAT1 and KAT2 suppress light- and low-CO 2 -induced stomatal open-
ing (Kwak et al. 2001 ; Lebaudy et al. 2008 ). These data provided genetic evi-
dences showing the importance of inward K + channels for stomatal opening, and
the presence of five different subunits in K + channel tetramers provide a regula-
tion mechanism for inward-rectifying K + channel activity. Another regulation
mechanism for K + channels is protein trafficking. ABA-induced internalization
of KAT1 was observed in Arabidopsis guard cells during stomatal closure, and
KAT1 can go back to the plasma membrane of guard cells for stomatal opening
(Sutter et al. 2007 ; Latorre et al. 2003 ). ABA can induce stomatal closure by acti-
vating outward K + channels and inhibiting inward K + channels simultaneously.
Using patch clamping technique, the inhibition of inward K + channel currents by
a pre-incubation of guard cell protoplast with ABA was observed in Arabidopsis
(Fan et al. 2008 ), supporting the inhibitory effects of ABA on inward K + chan-
nels. Interestingly, the inhibition of inward K + channels by the disruption of out-
ward anion channel SLAC1 was reported recently in Arabidopsis (Laanemets
et al. 2013 ; Wang et al. 2013 ), and the decrease of cytosolic Ca 2 + concentration
releases partially the inhibitory effects of the mutation of SLAC1 on inward K +