describe the role of abscisic acid in the closure of stomata during times of water stress, including the role of calcium ions as a second messenger

Published by Patrick Mutisya · 14 days ago

Cambridge A-Level Biology 9700 – Homeostasis in Plants

Homeostasis in Plants

Stomatal Regulation and Water Stress

Plants maintain internal water balance by regulating the aperture of stomata – microscopic pores on the leaf surface. When water availability declines, stomata close to reduce transpiration. The hormone abscisic acid (ABA) is the primary signal that initiates this response.

Role of Abscisic Acid (ABA)

ABA is synthesised in the chloroplasts of mesophyll cells when the leaf experiences a drop in water potential. The hormone then diffuses to the guard cells surrounding each stoma, where it triggers a cascade of intracellular events that lead to stomatal closure.

Signal Transduction Pathway

The sequence of events from ABA perception to stomatal closure can be summarised as follows:

  1. Water deficit → increased ABA synthesis in mesophyll cells.
  2. ABA moves through the apoplast to guard cells.
  3. ABA binds to PYR/PYL/RCAR receptors on the guard‑cell plasma membrane.
  4. Receptor activation inhibits PP2C phosphatases, allowing activation of SnRK2 kinases.
  5. SnRK2 kinases phosphorylate ion channels, causing an influx of Ca2+ from internal stores.
  6. Elevated cytosolic Ca2+ acts as a second messenger, activating downstream effectors.
  7. Activation of anion channels and outward‑rectifying K+ channels leads to loss of K+, Cl and organic acids from guard cells.
  8. Osmotic loss of solutes causes water to exit guard cells, reducing turgor pressure.
  9. Reduced turgor leads to stomatal pore closure.

Calcium Ions as a Second Messenger

Calcium ions (Ca2+) are central to the ABA‑induced signalling cascade. Their role can be broken down into three key functions:

  • Signal Amplification: A small rise in cytosolic Ca2+ triggers the opening of calcium‑dependent protein kinases (CDPKs) and calmodulin, which amplify the signal.
  • Channel Regulation: Phosphorylated CDPKs phosphorylate SLAC1 anion channels, increasing anion efflux and depolarising the guard‑cell membrane.
  • Cross‑Talk with Reactive Oxygen Species (ROS): Elevated Ca2+ stimulates NADPH oxidases, producing ROS that further modulate ion channel activity.

Key Molecular Players

ComponentFunction in Stomatal Closure
ABAHormonal signal produced under water stress; initiates signalling cascade.
PYR/PYL/RCAR receptorsBind ABA, inhibit PP2C phosphatases, allowing kinase activation.
SnRK2 kinasesPhosphorylate ion channels and calcium channels, raising cytosolic Ca2+.
Calcium ions (Ca2+)Second messenger; activates CDPKs and calmodulin.
SLAC1 anion channelFacilitates Cl and NO3 efflux, depolarising membrane.
GORK K+ channelOutward K+ efflux, loss of osmolytes.
NADPH oxidase (RBOH)Produces ROS that modulate channel activity.

Overall Effect on Guard‑Cell Turgor

The coordinated loss of anions, cations and water from guard cells reduces their internal osmotic potential. According to the equation for osmotic potential:

\$\Psi_s = -iCRT\$

where \$i\$ is the ionisation constant, \$C\$ the solute concentration, \$R\$ the gas constant and \$T\$ the absolute temperature, a decrease in \$C\$ makes \$\Psis\$ less negative, causing water to leave the cell. The resulting drop in turgor pressure (\$\Psip\$) forces the stomatal pore to close, conserving water.

Suggested diagram: ABA‑induced signalling pathway in guard cells, highlighting calcium influx and ion channel activation leading to stomatal closure.

Key Points for Revision

  • Water stress → increased ABA synthesis in mesophyll.
  • ABA binds to PYR/PYL/RCAR receptors on guard cells.
  • Signal transduction involves inhibition of PP2C, activation of SnRK2, and a rise in cytosolic Ca2+.
  • Ca2+ acts as a second messenger, activating CDPKs, calmodulin, and ROS production.
  • Activation of anion and K+ efflux channels leads to loss of solutes and water.
  • Reduced guard‑cell turgor causes stomatal closure, reducing transpiration.