FIGURE 1.

Schematic diagram of plant salt-stress sensors and signal transduction pathways involved in salt stress responses. High salt stress causes osmotic stress and ionic stress, both of which lead to the accumulation of ROS, triggering oxidative stress. (1) High concentrations of salt ions alter the concentration of ions in the cell wall, which are sensed by specific sensors or receptors (such as RLKs, GIPC, and FER), which activate signaling pathways such as the SOS pathway to redistribute ions and achieve ion homeostasis. (2) Changes in the balance between ion concentrations inside and outside the cell change the cell’s osmotic potential. The cell senses these changes through specific sensors (such as HPKs, NSCCs, and BON) and, through MAPK cascades (such as the HOG pathway), regulates the synthesis of organic osmolytes (such as proline and betaine) and the absorption of ions to achieve osmotic homeostasis. (3) The accumulation of ROS generated by plasma membrane–bound NADPH oxidase under salinity leads to secondary oxidative stress. Transcription factors such as CBF/DREB regulate the synthesis of some stress proteins (such as RD29A) to deal with the damage caused by secondary metabolites and achieve ROS homeostasis. Finally, salt tolerance is achieved through the synergy of various signaling pathways and the expression of salt tolerance–related genes. ROS, reactive oxygen species; RLKs, receptor-like protein kinases; GIPC, glycosyl inositol phosphorylceramide; FER, FERONIA; HPKs, histidine protein kinases; NSCCs, non-selective cation channels; BON, BONZAI1; SOS pathway, Salt Overly Sensitive pathway; MAPK cascades, mitogen-activated protein kinase cascades; HOG pathway, high-osmolarity glycerol pathway; NADPH, nicotinamide adenine dinucleotide phosphaten; CBF, CRT/DRE-binding factor; DREB, dehydration responsive element binding protein; ANN1, ANNEXIN1; CNGC, cyclic nucleotide-gated channel; GORK, Guard Cell Outward-Rectifying Potassium Channel; NHX, Na⁺/H⁺ exchanger.