Ion Channels in ABA Mediated Stomatal Regulation
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Ion Channels in ABA Mediated Stomatal Regulation
Plant growth and development are regulated by Internal Signals and by External Environmental Conditions. One important regulator that coordinates growth and development with responses to the environment is the Sesquiterpenoid hormone ABA (Abscisic Acid). ABA plays important roles in many cellular processes including Seed Development, Dormancy, Germination, Vegetative Growth, Leaf Senescence, Stomatal Closure, and Environmental Stress Responses.  ABA is synthesized in almost all cells, but its transport from roots to shoots and the recirculation of ABA in both Xylem and Phloem are important aspects of its physiological role. The most extensively investigated developmental and physiological effects of ABA are those involved in Seed Maturation and Dormancy and in the Regulation of Stomata. These diverse functions of ABA involve complex regulatory mechanisms that control its production, degradation, signal perception, and transduction (Ref.1).

During Drought Stress, a rapid response mediated by ABA is Stomatal Closure. Stomata are pores that open and close between pairs of specialized cells, termed "Guard Cells," in the epidermis of the aerial parts of plants. The hormone ABA triggers a signaling cascade in Guard Cells that results in Stomatal Closure and inhibits Stomatal Opening. Although both effects result in closed Stomata, they are not simple reversals of the same process. Several processes are involved in controlling Stomatal apertures. Among them, Ion Channel Regulation is one of the key mechanisms by which ABA controls Stomatal apertures. ABA controls three Plasmamembrane Ion Currents - two K+ (Potasium) currents IK, in (Kat1) and IK, out (GORK), and an Anion current ICl (Chloride) as well as the H+-ATPase and a hyperpolarisation-activated Ca2+ (Calcium) Channel (TPC1). ABA-induced Stomatal Closure is vital for plants to limit transpirational water loss during periods of drought. Inward Potassium channels in the Plasmamembrane mediate K+ uptake driving Stomatal Opening, while slow Anion Channels and Outward Potassium Channels mediate Solute loss driving Stomatal Closure (Ref.2).


Stomatal Closure is mediated by Turgor reduction in Guard Cells, which is caused by efflux of K+ and Anions from Guard Cells, Sucrose Removal, and a parallel conversion of the Organic Acid Malate to osmotically inactive Starch.  ABA triggers Cytosolic Calcium ((Ca2+) cyt) increase. In Guard Cells of A. thaliana, ABA-induced Ca2+ oscillations occur with a period of 10.3 min, and are therefore too slow to encode a signal that activates Anion channels with a lag time of 2 min. (Ca2+) cyt elevations activate two different types of Anion channels: S-Type (Slow-Activating Sustained) and R-Type (Rapid Transient) Anion channels. Both mediate Anion release from Guard Cells, causing Depolarization. This change in membrane potential deactivates K+in (Inward-Rectifying K+) channels such as Kat1 and activates K+out (Outward-Rectifying K+) channels such as GORK (Guard cell Outward Rectifying K(+) channel), resulting in K+ efflux from Guard Cells. In addition, ABA causes an alkalization of the Guard Cell cytosol, which directly enhances K+out channel activity and down-regulates the transient R-type Anion Channels. The sustained efflux of both Anions and K+ from Guard cells via Anion and K+out Channels contributes to loss of Guard Cell Turgor, which leads to Stomatal Closing.  As Vacuoles can take up over 90% of the Guard Cell’s volume, over 90% of the Ions exported from the Cell during Stomatal Closing are first transported from Vacuoles into the Cytosol. (Ca2+) cyt elevation activates VK (Vacuolar K+) Channels proposed to provide a pathway for Ca2+-induced K+ release from the vacuole. At resting (Ca2+) cyt, K+ efflux from Guard Cell vacuoles can be mediated by FV (Fast Vacuolar) Channels, allowing for versatile Vacuolar K+ efflux pathways. The pathways for anion release from vacuoles remain elusive (Ref.1 & 3).

Stomatal Opening relies on increases in K+, Cl, Malate2–, and Sucrose in the Guard Cell Symplast to drive water influx and cell swelling. These processes result in an outbowing of the Guard Cell pair and an increase in pore aperture. Stomatal opening is driven by Plasma membrane proton-extruding H+-ATPase . H+-ATPase can drive K+ uptake via K+in channels. During inhibition of Stomatal opening by the plant hormone ABA, these channels are inhibited. Cytosolic Ca2+ elevations in guard cells down-regulate both K+in channels and plasma membrane H+-ATPase , providing a mechanistic basis for ABA and Ca2+ inhibition of K+ uptake during Stomatal Opening (Ref.4). Recent efforts have led to major advances in understanding the molecular mechanisms of Guard Cell ABA Signaling. A model for the functions of Ion channels in regulating stomatal movements has provided a framework for the characterization of new, early ABA transduction mechanisms. However, many components within the nonlinear and branched pathways of this network remain to be identified. Moreover, the relative positioning of the mechanisms identified and the exact functions of pharmacologically predicted transducers remain to be determined using combined Genetic, Cell Biological and Biophysical approaches (Ref.5).