Citrate exudation induced by aluminum is independent of plasma membrane H+-ATPase activity and coupled with potassium efflux from cluster roots of phosphorus-deficient white lupin

Abstract

Exudation of organic acid anions is one of the mechanisms responsible for aluminum (Al) tolerance. The plasma membrane (PM) H+-ATPase is involved in the exudation of organic acid anions. However, the relationship between organic acid exudation and PM H+-ATPase under Al toxicity remains unclear. This study aims to investigate the correlation among Al-induced citrate exudation, PM H+-ATPase activity and counterions for citrate release from cluster roots of phosphorus-deficient (−P) white lupin. Al and various pharmacological agents were applied to incubate the cluster roots of P-deficient white lupin; the citrate exudation rate, PM H+-ATPase activity and ion exudation of cluster roots were examined. Citrate exudation from cluster roots of P-deficient white lupin was induced by 50 μM Al treatment within 1.5 h, but no extra increase was found when the duration of Al treatment increased. The PM H+-ATPase activity of cluster roots was insensitive to Al treatment, irrespective of Al concentration and duration of Al treatment. Al treatment increased K+ efflux but not H+ efflux from cluster roots. After application of pharmacological agents to P-deficient cluster roots under Al treatment or not, vanadate decreased H+ efflux and increased K+ efflux, but had no inhibitory effect on citrate exudation; fusicoccin increased H+ efflux and citrate exudation, but decreased K+ efflux; tetraethylammonium (TEA) chloride, a K+-channel inhibitor, inhibited K+ efflux and increased H+ efflux. These results indicate that citrate exudation induced by combined treatment with P-deficiency and Al is independent of PM H+-ATPase activity, and is coupled with K+ efflux, which may compensate H+ efflux for keeping the charge balance for Al-induced citrate exudation from cluster roots of P-deficient white lupin.