Figure 2.

Regulation of ion transport across the plasma membrane by polyamines and their catabolites. (1) PAs are exported from the cytosol to the apoplast against the electrochemical gradient. (2) PAs inhibit K⁺ (inward-rectifying, KIRC and outward rectifying, KORC) and non-selective voltage-independent cation (VI-NSCC) channels. (3) PAs oxidation by diamine (DAO) and/or polyamine (PAO) oxidases generates H₂O₂ in the apoplastic space. There H₂O₂ can be converted to •OH by the single electron reduction catalyzed by transient valency metal ions. (4) H₂O₂ and •OH activate a variety of non-selective Ca²⁺-permeable channels, including hyperpolarization-activated Ca²⁺ influx channel (HACC), annexin-formed channel (ANN), and non-selective voltage-independent conductance (ROSIC). (5) H₂O_2, released during PAs catabolization, causes a rapid NO generation. In its turn, NO inhibits KORC by a direct nitrosylation and in1duces the intracellular Ca²⁺ release via a pathway involving cGMP and cyclic adenosine ribose (cADPR). (6) Ca²⁺-sensitive network. Several PM channels, including slow anion channel (SLAC) and pumps, are regulated by cytosolic Ca²⁺. (7) PAs potentiate the ROSIC activation, activate the PM Ca²⁺-ATPase and alter the activity of the PM H⁺-ATPase.