The BIG protein distinguishes the process of CO (2)‐induced stomatal closure from the inhibition of stomatal opening by CO (2)

We conducted an infrared thermal imaging‐based genetic screen to identify Arabidopsis mutants displaying aberrant stomatal behavior in response to elevated concentrations of CO (2). This approach resulted in the isolation of a novel allele of the Arabidopsis BIG locus (At3g02260) that we have called CO (2) insensitive 1 (cis1). BIG mutants are compromised in elevated CO (2)‐induced stomatal closure and bicarbonate activation of S‐type anion channel currents. In contrast with the wild‐type, they fail to exhibit reductions in stomatal density and index when grown in elevated CO (2). However, like the wild‐type, BIG mutants display inhibition of stomatal opening when exposed to elevated CO (2). BIG mutants also display wild‐type stomatal aperture responses to the closure‐inducing stimulus abscisic acid (ABA). Our results indicate that BIG is a signaling component involved in the elevated CO (2)‐mediated control of stomatal development. In the control of stomatal aperture by CO (2), BIG is only required in elevated CO (2)‐induced closure and not in the inhibition of stomatal opening by this environmental signal. These data show that, at the molecular level, the CO (2)‐mediated inhibition of opening and promotion of stomatal closure signaling pathways are separable and BIG represents a distinguishing element in these two CO (2)‐mediated responses.