Abstract
The stress hormone abscisic acid (ABA) induces expression of defence genes in many organs, modulates ion homeostasis and metabolism in guard cells, and inhibits germination and seedling growth. Concerning the latter effect, several mutants of Arabidopsis thaliana with improved capability for H(+) efflux (wat1-1D, overexpression of AKT1 and ost2-1D) are less sensitive to inhibition by ABA than the wild type. This suggested that ABA could inhibit H(+) efflux (H(+)-ATPase) and induce cytosolic acidification as a mechanism of growth inhibition. Measurements to test this hypothesis could not be done in germinating seeds and we used roots as the most convenient system. ABA inhibited the root plasma-membrane H(+)-ATPase measured in vitro (ATP hydrolysis by isolated vesicles) and in vivo (H(+) efflux from seedling roots). This inhibition involved the core ABA signalling elements: PYR/PYL/RCAR ABA receptors, ABA-inhibited protein phosphatases (HAB1), and ABA-activated protein kinases (SnRK2.2 and SnRK2.3). Electrophysiological measurements in root epidermal cells indicated that ABA, acting through the PYR/PYL/RCAR receptors, induced membrane hyperpolarization (due to K(+) efflux through the GORK channel) and cytosolic acidification. This acidification was not observed in the wat1-1D mutant. The mechanism of inhibition of the H(+)-ATPase by ABA and its effects on cytosolic pH and membrane potential in roots were different from those in guard cells. ABA did not affect the in vivo phosphorylation level of the known activating site (penultimate threonine) of H(+)-ATPase in roots, and SnRK2.2 phosphorylated in vitro the C-terminal regulatory domain of H(+)-ATPase while the guard-cell kinase SnRK2.6/OST1 did not.
Highlights
The hormone abscisic acid (ABA) plays a critical role in plant stress responses by transcriptional induction of defence genes in different organs
Recent results in Arabidopsis thaliana (Arabidopsis) indicate that the same core signal transduction pathway operates in both cases, with ABA bound to PYR/PYL/RCAR (PYRABACTIN RESISTANCE1 / PYR1-LIKE/ REGULATORY COMPONENTS OF ABA RECEPTORS; hereafter referred to as PYR/PYL) receptors inhibiting clade A of protein phosphatase type 2C (PP2C) protein phosphatases (ABI1, ABI2, HAB1, and PP2CA) and resulting in activation of a subgroup of SnRK2 protein kinases (2.2, 2.3 and guard-cell OST1/2.6)
These results suggested that one mechanism of inhibition of growth by ABA at this stage could be cytosolic acidification
Summary
The hormone abscisic acid (ABA) plays a critical role in plant stress responses by transcriptional induction of defence genes in different organs. During the closing of stomata, ABA has a non-transcriptional mechanism modulating ion homeostasis and resulting in inhibition of plasma membrane (PM) H+-ATPase, membrane depolarization, cytosolic alkalinisation, and efflux of K+ and anions (Fujii et al, 2009; Kim et al, 2010; Joshi-Saha et al, 2011). The PM H+-ATPase of guard cells is inhibited by ABA through a pathway involving the kinase OST1/SnRK2.6 (Merlot et al, 2007). This results in dephosphorylation of the activating site of the PM H+-ATPase (penultimate threonine-947; Yin et al, 2013) by an unknown mechanism
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