Abstract

Elevated carbon dioxide (CO2) has been shown to enhance the photosynthesis of plants, while inducing stomatal closure in leaves. Stomatal closure is always a key issue regarding plants’ responses against stress under elevated CO2. This paper examined the mechanism underlying CO2 elevation-induced stomatal closure in Arabidopsis. Endogenous nitric oxide (NO) in guard cells was detected by the specific probe 4-amino-5-methylamino-2′,7′-difluorofluorescein diacetate. The Arabidopsis wild type, nitric oxide synthase (NOS) mutant atnos1, and nitrate reductase (NR) mutant nia1nia2 were used as experimental materials. The present study shows that elevated CO2-induced NO accumulation in guard cells by 120 % and decreased the aperture of stomata by 32 % compared with ambient CO2. CO2 elevation-induced stomatal closure was reversed by scavenging NO. Here, we suggested that NO plays an important role in stomatal closure of Arabidopsis induced by elevated CO2. The pharmacological and genetic evidence shows that both the NOS inhibitor L-NAME and NR inhibitor tungstate significantly decreased NO accumulation in guard cells and inhibited stomatal closure, whereas the stomatal aperture of both the atnos1 and nia1nia2 mutants decreased slightly under elevated CO2, indicated that both NOS-like and NR were involved in CO2 elevation-induced NO accumulation. Therefore, we conclude from these findings that elevated CO2 increases the level of NO through both NOS-like and NR, which then induces stomatal closure in Arabidopsis under elevated CO2.

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