The Responce Of Calcium Ions To Abscisic Acid In Relation To Guard Cell Closure

"A discussion of the role of Ca2+ in the response of stomatal guard cells to ABA'lt;/p>

Abscisic acid (ABA) induced calcium ion (Ca2+) flux is responcible for the decrease in turgor pressure in stomatal guard cells (McAinsh et Al 1997). (Ca2+) signalling mediates changes in (Malate2-), (Cl-) and (K+) concentration within the cell cytosol via the activation and inhibition of different membrane bound ion channels.

(Ca2+) interacts with kinases in a signal cascade induced by the activation of the ABA and RCAR-ABI1 heterotrimeric receptor complex (Raghavendra et Al, 2010). The activation of the ABA receptor triggers H2O2 production in the guard cells (Pei et Al, 2000), leading to the activation and opening of voltage gated and selective stretch mediated (Ca2+) channels in the membrane causing an influx of (Ca2+)in into the cytosol (McAinsh et Al, 1997), resulting in the initial depolarisation of the cell membrane. Increase (Ca2+)cyt concentration has a rage of implications for cell processes. Firstly, the increase in (Ca2+)cyt causes a positive feedback effect involving selective voltage gated slow vacuolar (SV) channels (McAinsh e Al, 1997), which open to allow an efflux of (Ca2+)out into the cytosol, amplifying the initial membrane depolarisation.

The rapid increase in (Ca2+)cyt causes (K+)in inhibition through the blocking of the KAT1 inward recifying ion channel (Shroeder and Fang, 1991), via interaction with ABI5-ABFs and ABI4-AP2 kinases, resulting in the decreased influx of (K+)in (McAinsh et Al, 1997). Furthermore, high levels of (Ca2+)cyt causes H+-ATPase (V-ATPase) inhibition. This reduces the overall efflux of (Ca2+) out of the cell (McAinsh et Al, 1997), causing further membrane depolarisation (Boutry and Boutry, 1995). Due to this the depolarisation sensitive outward rectifying (K+) channel in the cell membrane is activated and causes the efflux of (K+)out (Shroeder et Al 1987, Schroeder and Fang, 1991). High concentrations of (Ca2+)cyt activate the (K+) vacuolar (VK) channels in the vacuolar membrane, which leads to (K+)out efflux into the cytosol (McAinsh et Al, 1997). These ions are then removed by the active outward rectifying membrane bound (K+) channel .

Additionally, ABA induced increase in (Ca2+)cyt acts on the movement of (Cl-)out and (Malate2-)out, by the activation of membrane bound S-Type anion channels, for example OST1, via sphingsine-1-phosphate (S1P) and associated kinases (Pandey et Al, 2007). This leads to membrane depolarisation as the OST1 anion channel is permeable to both (Cl-)out and (Malate2-)out. This coupled with the inhibited V-ATPase pump acts to amplify the depolarisation effect of (Ca2+)cyt, thereby perpetuating the efflux of (K+)out, (Malate2-)out and (Cl-)out, and therefore reducing the turgor pressure of the guard cells.

The overall response of (Ca2+) to ABA is a dramatic increase in (Ca2+)cyt concentration, resulting in the efflux of (Cl-) and (Malate2-) anions as well as (K+) cations, via interactions with both cation and anion channels in the cell and vacuolar membranes. This brings about a decrease in guard cell turgor, resulting in the reduction of stomatal aperture.