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Plant Physiol, December 1999, Vol. 121, pp. 1375-1382
Early Copper-Induced Leakage of K+ from Arabidopsis
Seedlings Is Mediated by Ion Channels and Coupled to Citrate
Efflux1
Angus S.
Murphy,
William R.
Eisinger,
Jon E.
Shaff,
Leon V.
Kochian, and
Lincoln
Taiz*
Department of Biology, University of California, Santa Cruz,
California 95064 (A.S.M., L.T.); Department of Biology, Santa Clara
University, Santa Clara, California 95053 (W.R.E.); and United States
Plant, Soil, and Nutrition Lab, United States Department of
Agriculture-Agricultural Research Service, Cornell University,
Ithaca, New York 14853 (J.E.S., L.V.K.)
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 86Rb+ 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.
1
This research was supported by grant nos.
94-37100-0755 (to A.M. and L.T.) and 98-35100-6105 (J.S. and L.K.)
from the U.S. Department of Agriculture.
*
Corresponding author; e-mail taiz{at}biology.ucsc.edu; fax
831-459-3139.
© 1999 American Society of Plant Physiologists
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