FIGURE 1.

A possible Ca²⁺-ROS signaling network involved in osmotic responses under salinity stress in root cells. Salinity stress causes osmotic shock to trigger the activation of PM MS Ca²⁺-permeable channels and Ca²⁺ influx. Elevated [Ca²⁺]_cyt leads to activation of various Ca²⁺ sensor proteins including CaMs, CMLs, CBLs, CDPKs as well as the ROS-producing enzyme, Noxs/Rbohs that are synergistically activated by Ca²⁺ binding and phosphorylation by Ca²⁺-dependent protein kinases such as CDPKs and CBL–CIPK complexes. Elevated apoplastic ROS activates ROS-activated PM Ca²⁺-permeable channels to trigger further Ca²⁺ influx, while Ca²⁺-permeable endomembrane channels/transporters may also been activated to sustain further Ca²⁺ mobilization. Elevated [Ca²⁺]_cyt may trigger downstream events such as activation of SOS1 and NHX1, Na⁺/H⁺ exchangers that transport cytosolic Na⁺, regulation of xylem loading of Na⁺, induction of osmolytes and osmo-protective proteins, and the retention of cytosolic ion balance. Ca²⁺-dependent protein kinases activated by elevated [Ca²⁺]_cyt mediate downstream events including expression of genes encoding proteins such as SOS1, antioxidant enzymes, osmolytes-biosynthetic enzymes as well as CaMs as signal amplifiers. Elevated [Ca²⁺]_cyt is reverted by the orchestrated action of active transporters such as Ca²⁺ exchangers and Ca²⁺-ATPases at the PM and tonoplast. H₂O₂ is transported to the cytosol by PM aquaporins to modify the cysteine residues of target proteins, thereby promoting redox signaling to regulate gene expression. Broken arrows indicate hypothetical links. ACA, autoinhibited Ca²⁺-ATPase; PA, polyamine; PAO, polyamine oxidase.