Article: article from journal or magazin.
The fou2 mutation in the major vacuolar cation channel TPC1 confers tolerance to inhibitory luminal calcium.
The Plant journal
Publication types: Journal Article ; Research Support, Non-U.S. Gov't Publication Status: ppublish
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 Ca2+ signals and cytosolic Ca2+ 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 Ca2+ sensitivity and Ca2+ impermeability. K+ fluxes through wild-type TPC1 were reduced or even completely faded away when vacuolar Ca2+ reached the 0.1-mm level. The fou2 protein under these conditions, however, remained active. Thus, D454N seems to be part of a luminal Ca2+ recognition site. Thereby the SV channel mutant gains tolerance towards elevated luminal Ca2+. 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 Ca2+ signals resulting in overproduction of jasmonate.
Arabidopsis/genetics, Arabidopsis/metabolism, Arabidopsis Proteins/genetics, Arabidopsis Proteins/metabolism, Calcium/metabolism, Calcium Channels/genetics, Calcium Channels/metabolism, Calcium Signaling, Cytosol/metabolism, Gene Expression Regulation, Plant, Membrane Potentials, Patch-Clamp Techniques, Point Mutation, Potassium/metabolism, Vacuoles/metabolism, Vacuoles/physiology
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