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

Chater, Caspar; Peng, Kai; Movahedi, Mahsa; Dunn, Jessica A.; Walker, Heather J.; Liang, Yun-Kuan; McLachlan, Deirdre H.; Casson, Stuart; Isner, Jean Charles; Wilson, Ian; Neill, Steven J.; Hedrich, Rainer; Gray, Julie E.; Hetherington, Alistair M.

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


Authors

Caspar Chater

Kai Peng

Mahsa Movahedi

Jessica A. Dunn

Heather J. Walker

Yun-Kuan Liang

Deirdre H. McLachlan

Stuart Casson

Jean Charles Isner

Steven J. Neill

Rainer Hedrich

Julie E. Gray

Alistair M. Hetherington



Abstract

© 2015 The Authors. 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.

Journal Article Type Article
Acceptance Date Sep 2, 2015
Online Publication Date Oct 8, 2015
Publication Date Oct 19, 2015
Deposit Date Dec 2, 2015
Publicly Available Date Feb 25, 2016
Journal Current Biology
Print ISSN 0960-9822
Publisher Elsevier (Cell Press)
Peer Reviewed Peer Reviewed
Volume 25
Issue 20
Pages 2709-2716
DOI https://doi.org/10.1016/j.cub.2015.09.013
Keywords guard cells; stomata; ABA receptors; [CO2] signaling; ABA signaling; NADPH oxidases; Rboh genes; signaling convergence; ROS; stomatal closure; stomatal density
Public URL https://uwe-repository.worktribe.com/output/804515
Publisher URL http://dx.doi.org/10.1016/j.cub.2015.09.013
Contract Date Feb 25, 2016

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