Fusicoccin counteracts the toxic effect of cadmium on the growth of maize coleoptile segments

Abstract

The effects of cadmium (Cd; 0.1–1000 lM) and fusicoccin (FC) on growth, Cd2? content, and membrane potential (Em) in maize coleoptile segments were studied. In addition, the Em changes and accumulation of Cd and calcium (Ca) in coleoptile segments treated with Cd2? combined with 1 lM FC or 30 mM tetraethylammonium (TEA) chloride (K?-channel blocker) were also determined. In this study, the effects of Ca2?-channel blockers [lanthanum (La) and verapamil (Ver)] on growth and content of Cd2? and Ca2? in coleoptile segments were also investigated. It was found that Cd at high concentrations (100 and 1000 lM) significantly inhibited endogenous growth of coleoptile segments and simultaneously measured proton extrusion. FC combined with Cd2? counteracted the toxic effect of Cd2? on endogenous growth and significantly decreased Cd2? content (not the case for Cd2? at the highest concentration) in coleoptile segments. Addition of Cd to the control medium caused depolarization of Em, the extent of which was dependent on Cd concentration and time of treatment with Cd2?. Hyperpolarization of Em induced by FC was suppressed in the presence of Cd2? at 1000 lM but not Cd2? at 100 lM. It was also found that treatment of maize coleoptile segments with 30 mM TEA chloride caused hyperpolarization of Em and decreased Cd2? content in coleoptile segments, suggesting that, in the same way as for FC, accumulation of Cd2? was dependent on plasma membrane (PM) hyperpolarization. Similar to FC, TEA chloride also decreased Ca2? content in coleoptile segments. La and Ver combined with Cd2? (100 lM) significantly decreased Cd content in maize coleoptile segments, but only La completely abolished the toxic effect of Cd2? on endogenous growth and growth in the presence of FC. Taken together, these results suggest that the mechanism by which FC counteracts the toxic effect of Cd2? (except at 1000 lM Cd2?) on the growth of maize coleoptile segments involves both stimulation of PM H?-ATPase activity by FC as well as Cd2?- permeable, voltage-dependent Ca channels, which are blocked by FC and TEA chloride-induced PM hyperpolarization.