Fig. 2.

Cumulative effect of elevated CO₂ and drought on stomatal behavior.

Increased CO₂ modulates OPEN STOMATA1 through ABA-dependent and ABA-independent mechanisms via increased NOX, ROS production and modulation of ion channel activities which in turn changes osmotic regulation, pH, protein phosphorylation and turgor pressure of guard cells. Additionally, increased rate of photosynthesis and ATP production show an additive effect on leaf enlargement and canopy temperature.

The molecular mechanisms underlying elevated CO₂-induced closure and reduction in stomatal density involve generation of reactive oxygen species. The pathway essentially has a bifurcation involving ABA and PYR/RCAR family of ABA receptors through guard cell ABA signaling pathway, acting through a loop-mediated mechanism where CO₂ induced an increase in ABA, which in turn increases the sensitivity of the system to elevated CO₂. CO₂ signal transduction pathway via ABA-OST1/SnRK2.6 shows that basal ABA signaling and OST1/SnRK2.6 are required to facilitate stomatal response to elevated CO₂. Although ABA and increased CO₂ induce PYR/PYL/RCAR family of ABA receptors in a stimulus specific manner, in the responses to CO₂, PYL4 and PYL5 are crucial.