Abscisic Acid and Abiotic Stress Tolerance in Crop Plants

Abstract

Abiotic stress is a primary threat to fulfill the demand of agricultural production to feed the world in coming decades. Plants reduce growth and development process during stress conditions, which ultimately affect the yield. In stress conditions, plants develop various stress mechanism to face the magnitude of stress challenges, although that is not enough to protect them. Therefore, many strategies have been used to produce abiotic stress tolerance crop plants, among them, abscisic acid (ABA) phytohormone engineering could be one of the methods of choice. ABA is an isoprenoid phytohormone, which regulates various physiological processes ranging from stomatal opening to protein storage and provides adaptation to many stresses like drought, salt, and cold stresses. ABA is also called an important messenger that acts as the signaling mediator for regulating the adaptive response of plants to different environmental stress conditions. In this review, we will discuss the role of ABA in response to abiotic stress at the molecular level and ABA signaling. The review also deals with the effect of ABA in respect to gene expression.

Keywords: ABA signaling; abiotic stress; abscisic acid; gene expression; phytohormone.

FIGURE 1

Schematic representation of biosynthesis of ABA in plants. ABA is derived from β-carotene (C₄₀) through an oxidative cleavage reaction in plastids. The first step of ABA biosynthesis pathway is the conversion of zeaxanthin and antheraxanthin to all trans-violaxanthin, which will be catalyzed by zeaxanthin epoxidase (ZEP). Antheraxanthin is the intermediate product. All–trans-violaxanthin is converted to 9-cis-violaxanthin or 9′-cis-neoxanthin by the 9-cis-epoxy carotenoid dioxygenase (NCED), which yields a C15 intermediate product called xanthoxin. Then the product xanthoxin is exported to the cytosol (Nambara and Marion-Poll, 2005) where xanthoxin is converted to ABA. Xanthoxin is then converted into ABA by two enzymatic reactions. Finally, xanthoxin is converted to an ABA aldehyde by the enzyme, short-chain alcohol dehydrogenase/reductase (SDR), and then oxidation of the abscisic aldehyde to ABA is catalyzed by the abscisic aldehyde oxidase (AAO). (Modified from, Taylor et al., 2000; Finkelstein and Rock, 2002; Tuteja, 2007; Mehrotra et al., 2014).

FIGURE 2

The schematic representation of major ABA signaling pathway in plants with and without ABA presence. The core components in ABA signaling include ABA receptors (PYR/PYL/RCAR), PP2C phosphatases (negative regulators), and SnRK2 kinases (positive regulators). In the absence of ABA, PP2Cs associate with SnRK2s and prevent the activation of SnRK2s. The inactive SnRK2s are unable to phosphorylate downstream substrates, and thus signal transduction is not occurring. In the presence of ABA, PYR/PYL/RCAR receptors bind to ABA and interact with PP2Cs, which release SnRK2s. The SnRK2s are then activated by autophosphorylation of the activation loop. The active SnRK2s can phosphorylate downstream substrate proteins, including transcription factors, ion channels, and enzymes such as NADPH oxidases, thereby inducing ABA responses. SnRK2s are subjected to regulation by other protein kinases. A Raf-like kinase (B3-MAPKKK) has been shown to activate SnRK2 through phosphorylating the activation loop, whereas casein kinase 2 (CK2) can phosphorylate SnRK2’s carboxyl-terminal serine residues, thereby enhancing SnRK2-PP2C interaction and inactivating SnRK2. Catalytically active SnRK2 is shown in green and inactive SnRK2 is in red. ABF, ABA-responsive element binding factor; ABI5, ABA insensitive 5; AREB, ABA-responsive element binding protein; B3-MAPKKK, B3-group Raf-like MAP kinase kinase kinase; KAT1, potassium channel in Arabidopsis thaliana 1; PP2C, Protein phosphatase 2C; PYR, pyrabactin resistance; PYL, PYR-related; RCAR, regulatory component of ABA receptor; SLAC1, slow anion channel 1; SnRK2, sucrose nonfermenting-1-related protein kinase 2.