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Review
. 2015 Jul 6;16(7):15251-70.
doi: 10.3390/ijms160715251.

Function of ABA in Stomatal Defense against Biotic and Drought Stresses

Chae Woo Lim  1 , Woonhee Baek  2 , Jangho Jung  3 , Jung-Hyun Kim  4 , Sung Chul Lee  5
Affiliations
Review

Function of ABA in Stomatal Defense against Biotic and Drought Stresses

Chae Woo Lim et al. Int J Mol Sci. .

Abstract

The plant hormone abscisic acid (ABA) regulates many key processes involved in plant development and adaptation to biotic and abiotic stresses. Under stress conditions, plants synthesize ABA in various organs and initiate defense mechanisms, such as the regulation of stomatal aperture and expression of defense-related genes conferring resistance to environmental stresses. The regulation of stomatal opening and closure is important to pathogen defense and control of transpirational water loss. Recent studies using a combination of approaches, including genetics, physiology, and molecular biology, have contributed considerably to our understanding of ABA signal transduction. A number of proteins associated with ABA signaling and responses--especially ABA receptors--have been identified. ABA signal transduction initiates signal perception by ABA receptors and transfer via downstream proteins, including protein kinases and phosphatases. In the present review, we focus on the function of ABA in stomatal defense against biotic and abiotic stresses, through analysis of each ABA signal component and the relationships of these components in the complex network of interactions. In particular, two ABA signal pathway models in response to biotic and abiotic stress were proposed, from stress signaling to stomatal closure, involving the pyrabactin resistance (PYR)/PYR-like (PYL) or regulatory component of ABA receptor (RCAR) family proteins, 2C-type protein phosphatases, and SnRK2-type protein kinases.

Keywords: ABA receptor; PP2C; SnRK2; abscisic acid (ABA); biotic and abiotic stresses; stomatal immunity.

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Figures

Figure 1
Figure 1
Schematic representation of a possible mechanism underlying the antagonistic and synergistic role of abscisic acid (ABA) signaling in plant defense response at the pre-invasive and post-invasive stages of Arabidopsis thaliana–Pseudomonas syringae interaction. At the pre-invasive stage, ABA signaling plays a synergistic role in plant resistance to P. syringae attack. Stomata constitute a major route of bacterial entry. Pathogen-associated molecular pattern (PAMP)-induced ABA signaling in the guard cells promotes stomatal closure and actively blocks P. syringae invasion [44,48]. This stomatal immunity involves the ABA receptor–2C-type protein phosphatase–open stomata 1 (RCAR-PP2C-OST1) complex acting as a core component of ABA signaling [12,44]. The phytotoxin coronatine (COR) is a virulence factor produced by P. syringae and it can compromise PAMP-induced stomatal defense by suppressing PAMP-induced ABA signaling and promoting stomatal reopening [12,44,49]. In contrast, ABA signaling plays an antagonistic role in post-invasive defense response. Pseudomonas syringae type III secreted effector (T3SE) proteins upregulate ABA biosynthesis and also the signaling pathways, thereby inhibiting the plant defense response [44,50]. In this process, ABA signaling antagonizes salicylic acid (SA)-mediated pathogenesis-related (PR) gene expression and callose deposition [12,48,50].
Figure 2
Figure 2
Simplified overview of stomatal movement via the abscisic acid (ABA) signaling pathway. Under normal conditions, 2C-type protein phosphatase (PP2C) family members, which are negative regulators of ABA signaling, suppress open stomata 1 (OST1) kinase activity via physical interaction, leaving the S-type anion channel (SLAC1) with basal activity. Under conditions of stress, including drought, the ABA concentration in leaves increases rapidly [9,10]. ABA perception occurs via regulatory component of ABA receptor (RCAR) family members functioning as ABA receptors in combination with PP2Cs [9,135]. The formation of the RCAR–PP2C complex breaks the PP2C–OST1 complex, thereby releasing active OST1 kinase from inhibition. In turn, OST1-mediated phosphorylation induces activation of the SLAC1 channel, thereby releasing anions and depolarizing the membrane [26]. This depolarization induces a further drop in turgor and closure of the stomatal pores.
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