Modulation of abscisic acid signaling for stomatal operation under salt stress conditions

Abstract

The plant hormone abscisic acid (ABA) triggers cellular tolerance responses to osmotic stress caused by high-salinity and water-deficient conditions. ABA controls the turgor pressure of guard cells in the plant epidermis through ionic fluxes via ion transporters anchored at the plasma membrane, leading to stomatal closure to limit transpiration and prevent the loss of water. However, stomatal apertures should be reversibly opened by a light signal to uptake carbon dioxide for photosynthesis, even under osmotic stress conditions. Plants utilize various strategies to regulate ABA-mediated stomatal closure in response to stressful conditions. Basically, plants regulate the accumulation of ABA, the signaling molecule induced in response to osmotic stress, during multiple metabolic processes (biosynthesis, catabolism, and conjugation) that occur in different subcellular organelles. In addition, the ABA signaling pathway in guard cells is modulated by ABA-dependent physical interactions among its core components, namely ABA molecules, receptors (e.g., pyrabactin resistance [PYR]/PYR1-like/regulatory components of ABA receptors), protein phosphatases (e.g., protein phosphatase type 2C), and kinases (e.g., sucrose non-fermenting-related protein kinase 2). Moreover, ABA induces the expression of numerous genes encoding proteins exerting either positive or negative effects on its accumulation, transportation, and signaling network. In parallel, the ABA signaling network can be desensitized by degradation of its core components via the ubiquitin-26S proteasome system or endocytic/vacuolar pathway in an ABA-dependent manner. This chapter details the mechanisms by which ABA constitutes a regulatory loop to finely tune its own homeostasis and signaling network, thereby modulating the stomatal operation.