Fig 5. The schematic diagram of some transporters and upregulated genes in the salt-tolerant mutant genotype.

It represents genes involved in salinity-stress signaling pathways and tolerant mechanisms in the salt-tolerant mutant genotype in response to 300 mM salt (six hours of exposure) in comparison to the wild-type genotype. After entrance of Na⁺ to cell cytoplasm, the activity of RBOH NADPH oxidase was increased to promote ROS formation and cytosolic Ca²⁺ content [101]. Ca²⁺ activated SOS3 and then SOS2, leading to SOS1-mediated Na⁺ extrusion [102]. On the other hand, NHX1 was activated by SOS3/SOS2 complex via HVA and HVP pumps, providing the driving force to sequester Na⁺ from cytosol to vacuole [103]. Moreover, TPK1/KCO1 is an important vacuolar permeable channel for K⁺ extrusion from vacuole to cytoplasm contributing to homeostasis regulation. Salt stress magnifies the activity of protein kinases in MAP kinase pathway to produce ethylene [104]. Ethylene can promote K⁺ retention through K⁺ channels, such as HAK and HKT to regulate Na⁺ and K⁺ homeostasis [15].