Abstract
The phytohormone abscisic acid (ABA) induces stomatal closure in response to drought stress, leading to reduction of transpirational water loss. A thiol tripeptide glutathione (GSH) is an important regulator of cellular redox homeostasis in plants. Although it has been shown that cellular redox state of guard cells controls ABA-mediated stomatal closure, roles of GSH in guard cell ABA signaling were largely unknown. Recently we demonstrated that GSH functions as a negative regulator of ABA signaling in guard cells. In this study we performed more detailed analyses to reveal how GSH regulates guard cell ABA signaling using the GSH-deficient Arabidopsis mutant cad2-1. The cad2-1 mutant exhibited reduced water loss from rosette leaves. Whole-cell current recording using patch clamp technique revealed that the cad2-1 mutation did not affect ABA regulation of S-type anion channels. We found enhanced activation of Ca2+ permeable channels by hydrogen peroxide (H2O2) in cad2-1 guard cells. The cad2-1 mutant showed enhanced H2O2-induced stomatal closure and significant increase of ROS accumulation in whole leaves in response to ABA. Our findings provide a new understanding of guard cell ABA signaling and a new strategy to improve plant drought tolerance.
Highlights
A phytohormone abscisic acid (ABA) induces closing of stomatal pores on leaf epidermis, resulting in reduction of transpirational water loss
THE cad2-1 MUTANT SHOWED ENHANCED DROUGHT TOLERANCE Previously we reported that GSH depletion by the cad2-1 mutation enhances ABA-induced stomatal closure in Arabidopsis (Okuma et al, 2011)
We confirmed that the cad2-1 mutation caused enhanced ABA-induced stomatal closure (Okuma et al, 2011) and reduction of water loss from leaves (Figure 1)
Summary
A phytohormone abscisic acid (ABA) induces closing of stomatal pores on leaf epidermis, resulting in reduction of transpirational water loss. It has been demonstrated that ABA activation of S-type anion channels is mediated via a cytosolic Ca2+-dependent pathway (Marten et al, 2007; Siegel et al, 2009). ABA activates hyperpolarization-activated Ca2+-permeable cation (ICa) channels in the plasma membrane of guard cells (Schroeder and Hagiwara, 1990; Hamilton et al, 2000; Pei et al, 2000; Kwak et al, 2003) and induces elevation of cytosolic free Ca2+ concentration ([Ca2+]cyt) in guard cells (McAinsh et al, 1990; Schroeder and Hagiwara, 1990; Gilroy et al, 1991; Allan et al, 1994; Grabov and Blatt, 1998; Allen et al, 1999; Marten et al, 2007). Electrophysiology experiments using Xenopus oocyte demonstrated that Arabidopsis CDPKs, CPK6, CPK21, and CPK23, directly phosphorylate and activate SLAC1 channel (Geiger et al, 2010; Brandt et al, 2012)
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