A New Insight of Salt Stress Signaling in Plant

Abstract

Many studies have been conducted to understand plant stress responses to salinity because irrigation-dependent salt accumulation compromises crop productivity and also to understand the mechanism through which some plants thrive under saline conditions. As mechanistic understanding has increased during the last decades, discovery-oriented approaches have begun to identify genetic determinants of salt tolerance. In addition to osmolytes, osmoprotectants, radical detoxification, ion transport systems, and changes in hormone levels and hormone-guided communications, the Salt Overly Sensitive (SOS) pathway has emerged to be a major defense mechanism. However, the mechanism by which the components of the SOS pathway are integrated to ultimately orchestrate plant-wide tolerance to salinity stress remains unclear. A higher-level control mechanism has recently emerged as a result of recognizing the involvement of GIGANTEA (GI), a protein involved in maintaining the plant circadian clock and control switch in flowering. The loss of GI function confers high tolerance to salt stress via its interaction with the components of the SOS pathway. The mechanism underlying this observation indicates the association between GI and the SOS pathway and thus, given the key influence of the circadian clock and the pathway on photoperiodic flowering, the association between GI and SOS can regulate growth and stress tolerance. In this review, we will analyze the components of the SOS pathways, with emphasis on the integration of components recognized as hallmarks of a halophytic lifestyle.

Keywords: GIGANTEA; NaCl; circadian clock; salinity; salt overly sensitive pathway.

Fig. 1.

A simplified model of plant cell sensing of stress, transduction of signals by transcriptional regulation, enzyme activity control, and translocational control. CYCLIC NUCLEOTIDE-GATED CHANNELS (CNGCs), GLUTAMATE RECEPTOR (GLR), NON-SELECTIVE CATION CHANNEL (NSCC), and HIGH AFFINITY K⁺ TRANSPORTER (HKT) mediate Na⁺ influx. SOS1 (plasma membrane Na⁺/H⁺ antiporter) is involved in the extrusion of Na⁺ from the cytoplasm and AtNHX1 mediates K⁺/H⁺ exchanges, involved in controlling the vacuolar osmotic potential and regulating cytosolic Na⁺-K⁺ ratio through vacuolar compartmentalization of K⁺.

Fig. 2.

GIGANTEA (GI) regulates flowering in a long day (A) and salt stress (B) response. (A) GI forms a complex with FKF1, which degrades CDF1, a repressor of CO, a central activator of photoperiodic flowering. Furthermore, GI independently promotes flowering of CO through miR172. miRNA172 targets AP2-like genes, such as TOE1, which negatively regulates multiple floral organ identity. SPY is considered a negative regulator of GA and positively promotes flowering during long days. (B) Salt-dependent interaction between GI and SOS2 (Kim et al., 2013). SOS2 and GI form a complex in unstressed plants. This complex prevents the interaction of SOS2 with SOS1; thus, SOS1 is kept in an inactive state. On salinity stress, the elevation of cellular Na⁺ triggers a salt stress-specific calcium signature, which is recognized by a calcium-binding protein, SOS3. SOS2 binds to calcium-bound SOS3, releasing the GI protein, which then is degraded. In turn, the free SOS2/SOS3 complex activates SOS1, a Na⁺/H⁺ antiporter, and sodium (Na⁺) ions are exported from the cells.