Molecular Insights Into Characterizing Guard Cell Responses to CO2.

It has been known for several decades that decreasing concentrations of CO₂ promote stomatal opening while increasing concentrations of CO₂ promote stomatal closure.  Given the rate at which anthropogenic carbon emissions are increasing atmospheric CO₂ concentrations, the molecular mechanisms by which guard cells sense and response to CO₂ are of great interest, particularly with regard to their impact on transpiration efficiency. This presentation will review the current status of our knowledge concerning CO₂ sensing in guard cells, and will discuss how the CO₂ signal is transduced into alterations in the fluxes of K⁺ and anions across the guard cell membrane that regulate guard cell turgor and thus stomatal aperture. Evidence will be presented for interaction between the guard cell CO₂ signaling cascade and other signals that regulate stomatal apertures, such as abscisic acid, which promotes stomatal closure, and light, which promotes stomatal opening.