Submitted to: Plant Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/11/1999
Publication Date: N/A
Citation: N/A Interpretive Summary: Heavy metal (Pb, Zn, Cd, Cu, Cr and Ni) contamination of soils poses serious problems to both human health and agriculture in the U.S. One of the primary sites of entry of toxic heavy metals into the food chain is via uptake into plants, with deposition in the edible portions. Thus, it is important that we understand and characterize the absorption, accumulation and tolerance to heavy metals in plants. Also, there is considerable current interest in using the ability of plants to absorb heavy metals from the soil as a way to clean up contaminated soils. Current engineering-based technologies used to remediate soils (e.g., removal of top soil for storage in landfills) are quite costly, and often dramatically disturb the landscape. Recently, there has been considerable interest focused on the use of terrestrial plants to absorb heavy metals from the soil and concentrate them in the easily harvestable shoot tissues as an alternative remediation technology. One limit to the development of this technology is our lack of understanding of heavy metal transport and tolerance processes in plants. In this paper, we report on a potentially new plant tolerance mechanism to Cu toxicity that involves specific Cu inhibition of the cytosolic enzyme, aconitase. This inhibition results in the increased accumulation and release from root cells of the organic acid citrate, which could chelate Cu in the soil solution and in root cells, thus minimizing its toxic effects.
Technical Abstract: Copper tolerance among Arabidopsis thaliana ecotypes is inversely correlated with long term K+ leakage and positively correlated with short term K+ leakage. 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. K+ channel blockers tetraethyl ammonium chloride (TEA) )and 4-aminopyridine (4-AP) both inhibited short-term copper-induced K+ efflux. In contrast, peroxide-induced K+ efflux was insensitive to both TEA and 4-AP. Copper-induced lipid peroxidation exhibited a lag time of 4 hours, while peroxide-induced lipid-peroxidation began immediately. The results suggest that channels mediate short-term copper-induced K+ efflux, whereas peroxide-induced K+ efflux primarily 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.