title: Heavy metal toxicity: cadmium permeates through calcium channels and disturbs the plant water status.
abstract: Because plant wilting has been described as a consequence of cadmium (Cd2+) toxicity, we investigate Cd2+ effects on plant water losses, gas exchanges and stomatal behaviour in Arabidopsis thaliana L. Effects of 1-week Cd2+ application in hydroponic condition (CdCl2 10-100 micro m) were analyzed. A 10- micro m Cd2+ concentration had no significant effect on the plant-water relationship and carbon assimilation. At higher Cd2+ concentrations, a Cd2+ -dependent decrease in leaf conductance and CO2 uptake was observed despite the photosynthetic apparatus appeared not to be affected as probed by fluorescence measurements. In epidermal strip bioassays, nanomolar Cd2+ concentrations reduced stomatal opening under light in A. thaliana, Vicia faba and Commelina communis. Application of 5 micro m ABA limited the root-to-shoot translocation of cadmium. However, the Cd2+-induced stomatal closure was likely ABA-independent, since a 5-day treatment with 50 micro m Cd2+ did not affect the plant relative water content. Additionally, a similar Cd2+-induced stomatal closure was observed in the ABA insensitive mutant abi1-1. Interestingly, this mutant displayed a higher transpiration rate than the wild type but did not accumulate more Cd2+, arguing that Cd2+ uptake is not dependent only on the transpiration flow. Application of putative calcium channels inhibitors suppressed the inhibitory effect of Cd2+ in epidermal strip experiments, suggesting that Cd2+ could enter the guard cell through calcium channels. Patch-clamp studies with V. faba guard cell protoplasts showed that plasma membrane K+ channels were insensitive to external Cd2+ application whereas Ca2+ channels were found permeable to Cd2+. In conclusion, we propose that Cd2+ affects guard cell regulation in an ABA-independent manner by entering the cytosol via Ca2+ channels.
authors.affiliation: CEA Cadarache, DSV-DEVM, Laboratoire des Echanges Membranaires et Signalisation, UMR 163 CEA-CNRS, Univ-mediterranée, BP1-F13108, St Paul-lez-Durance, France.
authors.forename: Laetitia
authors.initials: L
authors.lastname: Perfus-Barbeoch
authors.forename: Nathalie
authors.initials: N
authors.lastname: Leonhardt
authors.forename: Alain
authors.initials: A
authors.lastname: Vavasseur
authors.forename: Cyrille
authors.initials: C
authors.lastname: Forestier
mesh_terms: D000040:Abscisic Acid / Q000494:pharmacology; D017360:Arabidopsis / Q000187:drug effects* / Q000378:metabolism*; D019256:Cadmium Chloride / Q000378:metabolism* / Q000633:toxicity*; D015220:Calcium Channels / Q000378:metabolism*; D002245:Carbon Dioxide / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004553:Electric Conductivity; D017136:Ion Transport / Q000187:drug effects; D010788:Photosynthesis / Q000187:drug effects; D018515:Plant Leaves / Q000187:drug effects / Q000378:metabolism; D015221:Potassium Channels / Q000378:metabolism; D013997:Time Factors; D014867:Water / Q000378:metabolism*
chemical_list: D015220:Calcium Channels; D015221:Potassium Channels; D014867:Water; D002245:Carbon Dioxide; D000040:Abscisic Acid; D019256:Cadmium Chloride