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Curr Biol. 2015 Oct 19;25(20):2709-16. doi: 10.1016/j.cub.2015.09.013. Epub 2015 Oct 8.

Elevated CO2-Induced Responses in Stomata Require ABA and ABA Signaling.

Author information

1
Department of Molecular Biology and Biotechnology, University of Sheffield, Firth Court, Western Bank, Sheffield S10 2TN, UK.
2
School of Biological Sciences, Life Sciences Building, University of Bristol, Woodland Road, 24 Tyndall Avenue, Bristol BS8 1TQ, UK.
3
Department of Animal and Plant Sciences, University of Sheffield, Alfred Denny Building, Western Bank, Sheffield S10 2TN, UK.
4
State Key Laboratory of Hybrid Rice, College of Life Sciences, Wuhan University, Wuhan 430072, China.
5
Faculty of Health and Life Sciences, University of the West of England, Bristol Frenchay Campus, Coldharbour Lane, Bristol BS16 1QY, UK.
6
Institute for Molecular Plant Physiology and Biophysics, University of Würzburg, 97082 Würzburg, Germany.
7
Department of Molecular Biology and Biotechnology, University of Sheffield, Firth Court, Western Bank, Sheffield S10 2TN, UK. Electronic address: j.e.gray@sheffield.ac.uk.
8
School of Biological Sciences, Life Sciences Building, University of Bristol, Woodland Road, 24 Tyndall Avenue, Bristol BS8 1TQ, UK. Electronic address: alistair.hetherington@bristol.ac.uk.

Abstract

An integral part of global environment change is an increase in the atmospheric concentration of CO2 ([CO2]) [1]. Increased [CO2] reduces leaf stomatal apertures and density of stomata that plays out as reductions in evapotranspiration [2-4]. Surprisingly, given the importance of transpiration to the control of terrestrial water fluxes [5] and plant nutrient acquisition [6], we know comparatively little about the molecular components involved in the intracellular signaling pathways by which [CO2] controls stomatal development and function [7]. Here, we report that elevated [CO2]-induced closure and reductions in stomatal density require the generation of reactive oxygen species (ROS), thereby adding a new common element to these signaling pathways. We also show that the PYR/RCAR family of ABA receptors [8, 9] and ABA itself are required in both responses. Using genetic approaches, we show that ABA in guard cells or their precursors is sufficient to mediate the [CO2]-induced stomatal density response. Taken together, our results suggest that stomatal responses to increased [CO2] operate through the intermediacy of ABA. In the case of [CO2]-induced reductions in stomatal aperture, this occurs by accessing the guard cell ABA signaling pathway. In both [CO2]-mediated responses, our data are consistent with a mechanism in which ABA increases the sensitivity of the system to [CO2] but could also be explained by requirement for a CO2-induced increase in ABA biosynthesis specifically in the guard cell lineage. Furthermore, the dependency of stomatal [CO2] signaling on ABA suggests that the ABA pathway is, in evolutionary terms, likely to be ancestral.

KEYWORDS:

ABA receptors; ABA signaling; NADPH oxidases; ROS; Rboh genes; [CO(2)] signaling; guard cells; signaling convergence; stomata; stomatal closure; stomatal density

PMID:
26455301
PMCID:
PMC4612465
DOI:
10.1016/j.cub.2015.09.013
[Indexed for MEDLINE]
Free PMC Article

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