Caspar Chater
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.
Authors
Kai Peng
Mahsa Movahedi
Jessica A. Dunn
Heather J. Walker
Yun-Kuan Liang
Deirdre H. McLachlan
Stuart Casson
Jean Charles Isner
Ian Wilson Ian2.Wilson@uwe.ac.uk
Senior Lecturer
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.
Citation
Chater, C., Peng, K., Movahedi, M., Dunn, J. A., Walker, H. J., Liang, Y., …Hetherington, A. M. (2015). Elevated CO2-Induced Responses in Stomata Require ABA and ABA Signaling. Current Biology, 25(20), 2709-2716. https://doi.org/10.1016/j.cub.2015.09.013
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 |
Files
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