Figure 9. Schematic presentation of systematic Na₂CO₃ tolerance mechanisms in roots of Puccinellia tenuiflora.

Na₂CO₃ stress activates the modulation of Na⁺ influx restriction, Na⁺ compartmentalization, H⁺ transportation, glycine betaine accumulation, and vesicle trafficking in roots, which contribute to intracellular pH, ionic, and osmotic homeostasis. In addition, alkali stress leads to ROS burst in roots, resulting in the damages of root cell membrane. To alleviate ROS toxicity, specific ROS scavenging pathways (e.g., POD, GPX, and PrxR pathways) are induced in roots. Na₂CO₃ induces glycolysis, TCA cycle, and pentose phosphate pathway, providing energy, carbon skeletons, and NADPH for cellular metabolism in stressed roots. Importantly, Na₂CO₃ stress increases the Ca²⁺-mediated signaling pathway, activates the protein phosphorylation cascades, and subsequently triggers alkali-responsive gene expression. However, the protein synthesis, processing and destination are inhibited in roots under Na₂CO₃ stress. Solid line with arrow and “T” shape line represent stimulation and inhibition, respectively. The red words and green words indicate Na₂CO₃-induced and Na₂CO₃-reduced cellular processes, respectively. Dashed lines indicate indirect regulations. Abbreviations: GPX, glutathione peroxidase; MDA, malondialdehyde; POD, peroxidase; PrxR, peroxiredoxin; REL, relative electrolyte leakage; ROS, reactive oxygen species; TCA, tricarboxylic acid.