Arabidopsis Stomatal Response to Flemmating CO₂ and ABA

ABA Signaling Components in Stomatal Regulation

CO₂ Signaling Pathways and Integration with ABA

p35S:RCAR6 Construct

Molecular Mechanisms in F2 Lines During CO₂ Humidation Cycles

Central ABA Signaling Core: PYR/PYL/RCAR Receptors

PP2C Phosphatases: Negative Regulators

SnRK2 Protein Kinases: Positive Effectors

SLAC1 Anion Channels: Effector Targets

Calcium Signaling Integration

Reactive Oxygen Species (ROS) Signaling

1-4 members in Arabidopsis

Primary molecular sensors for ABA detection

Ligand-induced conformational change mechanism

Functional specialization

Guard cells: high RCAR isoform concentration

ABA binding mechanism

Subfamily I (PYR1, PYL1-PYL3)

Subfamily III (PYL4-PYL6, PYL7-PYL12)

ABA-dependent inhibitors of PP2C activity

Interact with PP2Cs (ABA-dependent & independent)

Clade A PP2C phosphatases

Six primary members

ABI1ABI2PP2CA/AHG3AHG1HAB1HAB2

Maintain inactive ABA signaling under non-stress

ABI1 & ABI2 crucial roles in stomatal regulation

Dephosphorylate OST1/SnRK2.6 (multiple sites)

Functional redundancy provides robustness

Loss of multiple PP2Cs -> increased ABA sensitivity

Directly dephosphorylate SLAC1 anion channels

SnRK1-RELATED PROTEIN KINASE 2 (SnRK2) family

Three ABA-responsive members

SnRK2.2SnRK2.3SnRK2.6/OST1 (predominant role in stomatal regulation)

OST1 activation

Relief from PP2C inhibition (ABA receptor-PP2C complexes)

Autophosphorylation at multiple sites

Primary target: SLAC1 anion channel

Basal activity in guard cells

Major anion channel for anion efflux

Unique voltage-gated ion channels

Activity primarily regulated by phosphorylation

Selectivity for physiological anions

SLAC1-mediated anion efflux

SnRK2s (OST1)

Calcium-dependent protein kinases (CPKs)Calcium B-like protein-interacting kinases (CIPKs)

Crucial secondary messenger

ABA triggers cytosolic calcium oscillations

Integration with core ABA pathway

ABA enhances SLAC1 calcium sensitivity (priming)

Requires intact ABA signaling (PYR/RCAR, PP2C inhibition)

CPKs activate SLAC1 independently of OST1

CPK21 and CPK23 directly phosphorylate SLAC1

molecular factors