Dataset Information

Abscisic acid-independent stomatal CO₂ signal transduction pathway and convergence of CO₂ and ABA signaling downstream of OST1 kinase.

ABSTRACT: Stomatal pore apertures are narrowing globally due to the continuing rise in atmospheric [CO₂]. CO₂ elevation and the plant hormone abscisic acid (ABA) both induce rapid stomatal closure. However, the underlying signal transduction mechanisms for CO₂/ABA interaction remain unclear. Two models have been considered: (i) CO₂ elevation enhances ABA concentrations and/or early ABA signaling in guard cells to induce stomatal closure and (ii) CO₂ signaling merges with ABA at OST1/SnRK2.6 protein kinase activation. Here we use genetics, ABA-reporter imaging, stomatal conductance, patch clamp, and biochemical analyses to investigate these models. The strong ABA biosynthesis mutants nced3/nced5 and aba2-1 remain responsive to CO₂ elevation. Rapid CO₂-triggered stomatal closure in PYR/RCAR ABA receptor quadruple and hextuple mutants is not disrupted but delayed. Time-resolved ABA concentration monitoring in guard cells using a FRET-based ABA-reporter, ABAleon2.15, and ABA reporter gene assays suggest that CO₂ elevation does not trigger [ABA] increases in guard cells, in contrast to control ABA exposures. Moreover, CO₂ activates guard cell S-type anion channels in nced3/nced5 and ABA receptor hextuple mutants. Unexpectedly, in-gel protein kinase assays show that unlike ABA, elevated CO₂ does not activate OST1/SnRK2 kinases in guard cells. The present study points to a model in which rapid CO₂ signal transduction leading to stomatal closure occurs via an ABA-independent pathway downstream of OST1/SnRK2.6. Basal ABA signaling and OST1/SnRK2 activity are required to facilitate the stomatal response to elevated CO₂ These findings provide insights into the interaction between CO₂/ABA signal transduction in light of the continuing rise in atmospheric [CO₂].

SUBMITTER: Hsu PK

PROVIDER: S-EPMC6196521 | biostudies-literature | 2018 Oct

REPOSITORIES: biostudies-literature

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Publications

Abscisic acid-independent stomatal CO2 signal transduction pathway and convergence of CO2 and ABA signaling downstream of OST1 kinase.

Hsu Po-Kai PK Takahashi Yohei Y Munemasa Shintaro S Merilo Ebe E Laanemets Kristiina K Waadt Rainer R Pater Dianne D Kollist Hannes H Schroeder Julian I JI

Proceedings of the National Academy of Sciences of the United States of America 20181003 42

Stomatal pore apertures are narrowing globally due to the continuing rise in atmospheric [CO2]. CO2 elevation and the plant hormone abscisic acid (ABA) both induce rapid stomatal closure. However, the underlying signal transduction mechanisms for CO2/ABA interaction remain unclear. Two models have been considered: (i) CO2 elevation enhances ABA concentrations and/or early ABA signaling in guard cells to induce stomatal closure and (ii) CO ...[more]

PMID: 30282744

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Project description:Stomatal pores play a central role in the control of carbon assimilation and plant water status. The guard cell pair that borders each pore integrates information from environmental and endogenous signals and accordingly swells or deflates, thereby increasing or decreasing the stomatal aperture. Prior research shows that there is a complex cellular network underlying this process. We have previously constructed a signal transduction network and a Boolean dynamic model describing stomatal closure in response to signals including the plant hormone abscisic acid (ABA), calcium or reactive oxygen species (ROS). Here, we improve the Boolean network model such that it captures the biologically expected response of the guard cell in the absence or following the removal of a closure-inducing signal such as ABA or external Ca2+. The expectation from the biological system is reversibility, i.e., the stomata should reopen after the closing signal is removed. We find that the model's reversibility is obstructed by the previously assumed persistent activity of four nodes. By introducing time-dependent Boolean functions for these nodes, the model recapitulates stomatal reopening following the removal of a signal. The previous version of the model predicts ∼20% closure in the absence of any signal due to uncertainty regarding the initial conditions of multiple network nodes. We systematically test and adjust these initial conditions to find the minimally restrictive combinations that appropriately result in open stomata in the absence of a closure signal. We support these results by an analysis of the successive stabilization of feedback motifs in the network, illuminating the system's dynamic progression toward the open or closed stomata state. This analysis particularly highlights the role of cytosolic calcium oscillations in causing and maintaining stomatal closure. Overall, we illustrate the strength of the Boolean network modeling framework to efficiently capture cellular phenotypes as emergent outcomes of intracellular biological processes.

Dataset Information

Abscisic acid-independent stomatal CO₂ signal transduction pathway and convergence of CO₂ and ABA signaling downstream of OST1 kinase.

Publications

Abscisic acid-independent stomatal CO<sub>2</sub> signal transduction pathway and convergence of CO<sub>2</sub> and ABA signaling downstream of OST1 kinase.

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