Fig. 1.

Metabolic and genetic properties of HT-PGPR involved in salt tolerance in plants. Metabolic and genetic properties of the HT-PGPR have a direct role in the amelioration of salt-stress in plants. They can regulate the expression of ion transporters/channels such as high-affinity K⁺ transporter (HKT1), Arabidopsis K⁺ Transporter 1(AKT1), Sodium Hydrogen Exchanger 2 (NHX2), weakly voltage‐dependent nonselective cation channel (NSCC), and plasma membrane intrinsic proteins (PIPs) that collectively take part in ion homeostasis and osmatic balance in plants. All of these channels/transporters can mediate Na⁺ and K⁺ influx into plant cells and help a suitable K+: Na+ ratio in the cytoplasm which prevents cellular damage and nutrient deficiency. The presence of HT-PGPR can also modulate the Salt Overly Sensitive (SOS1) pathways. Compatible osmolytes produced by HT-PGPR can be uptaken by plant cells to reduce the osmotic potential and stabilize proteins and cellular structures from salt stress. Volatile organic compounds (VOCs) produced by HT-PGPR can also trigger the induction of HKT1 in shoots and reduction of HKT1 in roots that limit Na⁺ entry into roots and facilitating shoot-to-root Na+ recirculation. Apart from these, non-enzymatic anti-oxidants produced by HT-PGPR can control the formation of ROS in plant cells. Excretion of exopolysaccharides (EPS) facilitate binding of Na+ in roots cells and prevents their translocation to leaves thus acting as a physical barrier around the roots.