Abstract

Summary The SV channel encoded by the TPC1 gene represents a Ca(2+)- and voltage-dependent vacuolar cation channel. Point mutation D454N within TPC1, named fou2 for fatty acid oxygenation upregulated 2, results in increased synthesis of the stress hormone jasmonate. As wounding causes Ca(2+) signals and cytosolic Ca(2+) is required for SV channel function, we here studied the Ca(2+)-dependent properties of this major vacuolar cation channel with Arabidopsis thaliana mesophyll vacuoles. In patch clamp measurements, wild-type and fou2 SV channels did not exhibit differences in cytosolic Ca(2+) sensitivity and Ca(2+) impermeability. K(+) fluxes through wild-type TPC1 were reduced or even completely faded away when vacuolar Ca(2+) reached the 0.1-mm level. The fou2 protein under these conditions, however, remained active. Thus, D454N seems to be part of a luminal Ca(2+) recognition site. Thereby the SV channel mutant gains tolerance towards elevated luminal Ca(2+). A three-fold higher vacuolar Ca/K ratio in the fou2 mutant relative to wild-type plants seems to indicate that fou2 can accumulate higher levels of vacuolar Ca(2+) before SV channel activity vanishes and K(+) homeostasis is impaired. In response to wounding fou2 plants might thus elicit strong vacuole-derived cytosolic Ca(2+) signals resulting in overproduction of jasmonate.