Simplified model for ABA signaling in stomatal guard cells. The net
effect is the loss of potassium and its anion (Cl– or malate2–) from the cell. (R =
receptor; ROS = reactive oxygen species; cADPR = cyclic ADP-ribose; G-protein =
GTP-binding protein; PLC = phospholipiase C

ABA binds to its receptors

ABA-binding induces the
formation of reactive oxygen
species, which activate plasma
membrane Ca2+ channels.

ABA increases the levels of
cyclic ADP-ribose and IP3,
which activate additional
calcium channels on the
tonoplast

The influx of calcium
initiates intracellular calcium
oscillations and promotes the
further release of calcium
from vacuoles.

The rise in intracellular
calcium blocks K+
in channels

The rise in intracellular
calcium promotes the
opening if Cl–
out (anion)
channels on the plasma
membrane, causing
membrane depolarization.

The plasma membrane
proton pump is inhibited by
the ABA-induced increase in
cytostolic calcium and a rise in
intracellular pH, further
depolarizing the membrane.

Membrane depolarization
activates K+
out channels.

K+ and anions to be
released across the plasma
membrane are first released
from vacuoles into the cytosol.