The BIG protein distinguishes the process of CO2 -induced stomatal closure from the inhibition of stomatal opening by CO2

BIG 蛋白可将 CO2 诱导的气孔关闭过程与 CO2 抑制的气孔开放过程区分开来

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作者:Jingjing He, Ruo-Xi Zhang, Kai Peng, Cecilia Tagliavia, Siwen Li, Shaowu Xue, Amy Liu, Honghong Hu, Jingbo Zhang, Katharine E Hubbard, Katrin Held, Martin R McAinsh, Julie E Gray, Jörg Kudla, Julian I Schroeder, Yun-Kuan Liang, Alistair M Hetherington

Abstract

We conducted an infrared thermal imaging-based genetic screen to identify Arabidopsis mutants displaying aberrant stomatal behavior in response to elevated concentrations of CO2 . This approach resulted in the isolation of a novel allele of the Arabidopsis BIG locus (At3g02260) that we have called CO2 insensitive 1 (cis1). BIG mutants are compromised in elevated CO2 -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 CO2 . However, like the wild-type, BIG mutants display inhibition of stomatal opening when exposed to elevated CO2 . 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 CO2 -mediated control of stomatal development. In the control of stomatal aperture by CO2 , BIG is only required in elevated CO2 -induced closure and not in the inhibition of stomatal opening by this environmental signal. These data show that, at the molecular level, the CO2 -mediated inhibition of opening and promotion of stomatal closure signaling pathways are separable and BIG represents a distinguishing element in these two CO2 -mediated responses.

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