Figure 1.

The dose-dependence of the vacuolar cation channels' block by intracellular polyamines and its implications for the salt stress resistance. Dose dependence for SV and FV channels at physiologically attainable (zero) tonoplast potential are drawn, using the values of blocking parameters from Brüggemann et al. (1998) and Dobrovinskaya et al., (1999a,b). Approximate ranges for intracellular PAs in plant cells are indicated by bars. At high salinity, efficient vacuolar Na⁺ sequestration is critical for the salt tolerance. This requires the increased Na⁺/H⁺ antiport activity and a decrease of Na⁺ leaks through non-selective FV and SV cation channels. The block by PAs would abolish the FV-mediated current, and strongly suppress the SV current. Continuous operation of the VK, weakly sensitive to PAs, acts as a shunt conductance for the electrogenic H⁺-pump, which fuels the active Na⁺ uptake, and contributes to the recuperation of the salt-induced cytosolic K⁺ loss. Salt stress stimulates expression of the cation-H⁺ antiporters, which may reduce the FV and SV activity via the increase of the luminal Ca²⁺. Over-expression of CAXs is also caused by the inhibition of the Spm⁴⁺ synthesis. Thus, PAs and vacuolar Ca²⁺ may act as alternative regulators of vacuolar cation channels.