Sensing of Salinity Stress and Intracellular Signalling

The overall response of a plant to salt stress is highly complex. It is not only removal of Na⁺ from the cytosol and the synthesis of osmolytes that are activated. The transcript abundance of up to several thousand genes changes within hours in the roots of plants exposed to toxic concentrations of NaCl. In A. thaliana the majority of these changes occur in the root cortex, where most of the Na⁺ accumulates (Deinlein et al. 2014).

Plant cells are able to separately sense the two components of salinity. Osmotic stress elicits responses distinct from those to ionic toxicity. The molecular nature of the sensors is still elusive (Fig. 7.34). A change in osmolality generates a stretch force on the plasma membrane, which may activate osmosensors. Mechanosensitive channels are known from yeast and other eukaryotes but not from plants.

The plant sensors are expected to be closely associated with Ca²⁺ channels. Cytosolic Ca²⁺ increases within seconds upon osmotic stress and represents the earliest documented response (also to other stresses such as cold; Chaps. 2 and 4). A recently identified hyperosmolalitygated calcium-permeable channel (OSCA1) is a candidate for an osmosensor (Yuan et al. 2014). Sensing of ionic stress caused by NaCl is less well understood.

The best-characterised salinity-specific signalling pathway is the one leading to the activation of the H⁺/Na⁺ antiporter SOS1 (Fig. 7.34). The elevated Ca²⁺ signal is sensed by the calcineurin B-like protein CBL4 (termed SOS3), which responds with dimerisation. The dimer can interact with the protein kinase CIPK24 (CBL- interacting protein kinase), known as SOS2. The SOS3/SOS2 complex is targeted at the plasma membrane, where it phosphorylates the SOS1 protein. Activation of this antiporter requires phosphorylation of its auto-inhibitory domain.

Calcium-dependent or calcium-controlled proteins (such as CBL4 or calmodulin) or protein kinases can transduce the salinity signal further downstream and trigger or attenuate gene expression (Fig. 7.34). Some of the calcium-dependent protein kinases regulate the response to abscisic acid (ABA), which accumulates under drought, as well as under salinity stress (Hirayama and Shinozaki 2010).

Fig. 7.38. Endogenous concentrations of abscisic acid (ABA) and methyl jasmonate (MeJA) in roots of rice plants subjected to salinity stress. a “Salt shock”—that is, transfer of seedlings from a NaCl-free medium to a NaCl-containing medium (150 mM). b ABA and methyl jasmonate content in rice seedlings after 2 days of treatment with different salt concentrations. c Water content in shoots after 2 days of exposure to salt stresses of different strengths

When a plant is subjected to a salt shock, a dramatic but transient increase in ABA takes place, which is similar to the reaction under drought (Fig. 7.38). Under prolonged salt stress the level of ABA might remain elevated or might return to close to the original concentration, depending on the plant species and plant organ, as well as on the experimental conditions. Part of this reaction might indeed be due to the osmotic stress imposed by high salinity. ABA signalling leads via transcription factors to the enhanced formation and accumulation of compatible solutes and protective proteins such as dehydrins.