How Plants Tolerate Salt Stress

Abstract

Soil salinization inhibits plant growth and seriously restricts food security and agricultural development. Excessive salt can cause ionic stress, osmotic stress, and ultimately oxidative stress in plants. Plants exclude excess salt from their cells to help maintain ionic homeostasis and stimulate phytohormone signaling pathways, thereby balancing growth and stress tolerance to enhance their survival. Continuous innovations in scientific research techniques have allowed great strides in understanding how plants actively resist salt stress. Here, we briefly summarize recent achievements in elucidating ionic homeostasis, osmotic stress regulation, oxidative stress regulation, and plant hormonal responses under salt stress. Such achievements lay the foundation for a comprehensive understanding of plant salt-tolerance mechanisms.

Keywords: SOS pathway; ionic stress; osmotic stress; oxidative stress; phytohormone; salt stress.

Figure 1

Ionic-stress signaling pathways that maintain ionic homeostasis and thereby help plants to adapt to salt stress. Under non-stress conditions (before salt stress (A)), plasma membrane (PM) H⁺-ATPase activity is repressed by PKS5; SOS2 kinase activity is repressed by PKS5, 14-3-3, ABI2, and GI; and SOS1 activity is inhibited by clade D PP2C (PP2C.D). Under salt stress (B), GIPC binds Na⁺, inducing an increase in calcium signaling. FER perceives changes in the cell wall under long-term salt stress and mediates calcium signaling. The calcium receptors SOS3 and SCaBP8 bind Ca²⁺, interacting with and activating SOS2, which then phosphorylates SOS1 to activate its Na⁺/H⁺ antiporter activity. Salt stress induces PA accumulation, which promotes the kinase activity of MPK6. MPK6 then phosphorylates SOS1 to enhance the activity of SOS1. At the same time, SCaBP8 inhibits PP2C.D to relieve the inhibition of SOS1 by PP2C.D. ANN modulation of calcium signaling under salt stress positively regulates SCaBP8-activated SOS2; under long-term salt stress, SOS2 phosphorylates ANN4 and represses its Ca²⁺ channel activity, creating a specific calcium signal for long-term stress. After salt stress (C), BIN2 phosphorylates SOS2 and inhibits its kinase activity, helping plants to recover from stress.

Figure 2

ROS signal transduction response to salt stress. Salt stress induces a rapid increase in ROS accumulation. Sensors perceive the elevated ROS and transduce the ROS signal to stimulate plant responses. MAPK signaling cascades receive ROS signals and regulate the activity of the SOS pathway and ROS scavengers to modulate ionic homeostasis and ROS homeostasis, respectively. MAPKs also regulate gene expression to modulate plant growth under salt stress.

Figure 3

Outline of antioxidant defense mechanisms in plants. SOD, superoxide dismutase; CAT, catalase; POX, peroxidase; AsA, ascorbate; DHA, dehydroascorbate; GSSG, oxidized glutathione; GSH, reduced glutathione; APX, ascorbate peroxidase; MDHA, monodehydroascorbate; MDHAR, monodehydroascorbate reductase; DHAR, dehydroascorbate reductase; GR, glutathione reductase; GST, glutathione S-transferase; GPX, glutathione peroxidase; PPO, polyphenol oxidase; PRX, peroxiredoxin; TRX, thioredoxin; NADPH, nicotinamide adenine dinucleotide phosphate; O, oxygen; H₂O₂, hydrogen peroxide; O2^•−, superoxide radical; R, aliphatic, aromatic, or heterocyclic group; X, sulfate, nitrite, or halide group; ROOH, hydroperoxides; -SH, thiolate; -SOH, sulfenic acid.