Early copper-induced leakage of K(+) from Arabidopsis seedlings is mediated by ion channels and coupled to citrate efflux.
Copper tolerance among Arabidopsis ecotypes is inversely correlated with long-term K(+) leakage and positively correlated with short-term K(+) leakage (A. Murphy, L. Taiz [1997] New Phytol 136: 211-222). To probe the mechanism of the early phase of K(+) efflux, we tested various channel blockers on copper and peroxide-induced K(+) efflux from seedling roots. The K(+) channel blockers tetraethyl ammonium chloride and 4-aminopyridine (4-AP) both inhibited short-term copper-induced K(+) efflux. In contrast, peroxide-induced K(+) efflux was insensitive to both tetraethyl ammonium chloride and 4-AP. Copper-induced lipid peroxidation exhibited a lag time of 4 h, while peroxide-induced lipid peroxidation began immediately. These results suggest that short-term copper-induced K(+) efflux is mediated by channels, while peroxide-induced K(+) efflux represents leakage through nonspecific lesions in the lipid bilayer. Tracer studies with (86)Rb(+) confirmed that copper promotes K(+) efflux rather than inhibiting K(+) uptake. Short-term K(+) release is electroneutral, since electrophysiological measurements indicated that copper does not cause membrane depolarization. Short-term K(+) efflux was accompanied by citrate release, and copper increased total citrate levels. Since citrate efflux was blocked by 4-AP, K(+) appears to serve as a counterion during copper-induced citrate efflux. As copper but not aluminum selectively induces citrate production and release, it is proposed that copper may inhibit a cytosolic form of aconitase.
Murphy
A S
AS
Department of Biology, University of California, Santa Cruz, California 95064, USA.
Eisinger
W R
WR
Shaff
J E
JE
Kochian
L V
LV
Taiz
L
L
D017878:4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid / Q000494:pharmacology; D015761:4-Aminopyridine / Q000494:pharmacology; D000154:Aconitate Hydratase / Q000037:antagonists & inhibitors / Q000378:metabolism; D017360:Arabidopsis / Q000187:drug effects / Q000502:physiology*; D001692:Biological Transport; D002951:Citrates / Q000378:metabolism*; D003300:Copper / Q000494:pharmacology*; D003600:Cytosol / Q000201:enzymology; D004594:Electrophysiology / Q000379:methods; D005707:Gallic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D007473:Ion Channels / Q000037:antagonists & inhibitors / Q000502:physiology*; D007700:Kinetics; D015227:Lipid Peroxidation / Q000187:drug effects; D008293:Malates / Q000378:metabolism; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009544:Niflumic Acid / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism*; D026902:Potassium Channel Blockers; D015221:Potassium Channels / Q000502:physiology*; D012413:Rubidium / Q000493:pharmacokinetics; D019789:Tetraethylammonium / Q000494:pharmacology; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D014268:Trifluoperazine / Q000494:pharmacology
D002951:Citrates; D007473:Ion Channels; D008293:Malates; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D017392:Thiobarbituric Acid Reactive Substances; D014268:Trifluoperazine; D009544:Niflumic Acid; C006014:8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate; D005707:Gallic Acid; D019789:Tetraethylammonium; D003300:Copper; D015761:4-Aminopyridine; D000154:Aconitate Hydratase; D012413:Rubidium; D017878:4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid; D011188:Potassium