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Plant Physiology Preview Published on January 23, 2009; 10.1104/pp.108.133348
Received November 27, 2008 Nitric oxide contributes to cadmium toxicity in Arabidopsis thaliana by promoting cadmium accumulation in roots and by up-regulating genes related to iron uptake
UMR INRA 1088/CNRS 5184/Universite de Bourgogne, Plante-Microbe-Environnement, 21065 Dijon cedex, France; UMR 118 Amelioration des Plantes et Biotechnologies Vegetales, INRA/Agrocampus Rennes/Universite Rennes 1, BP 35327, 35653 Le Rheu cedex, France; the Laboratoire de Bioenergetique et Biotechnologie des Bacteries et Microalgues, SBVME, IBEB, DSV, CEA, CNRS, Universite Aix Marseille, 13108 Saint Paul lez Durance, France; the Laboratoire de Biochimie et Physiologie Moleculaire des Plantes, UMR 5004 Agro-M/CNRS/INRA/UMII, 34060 Montpellier cedex 1, France; Unite de Recherche en Genomique Vegetale, UMR 8114 CNRS/INRA/Universite d'Evry-Val d'Essonne, CP5708-91057 Evry, France * Corresponding author; email: wendehen{at}dijon.inra.fr.
Nitric oxide (NO) functions as a cell-signalling molecule in plants. In particular, a role for NO in the regulation of iron homeostasis and in the plant response to toxic metals has been proposed. Here, we investigated the synthesis and the role of NO in plants exposed to cadmium (Cd2+), a non-essential and toxic metal. We demonstrate that Cd2+ induces NO synthesis in roots and leaves of A. thaliana seedlings. This production, which is sensitive to nitric oxide synthase inhibitors, does not involve nitrate reductase and AtNOA1 but requires IRT1 encoding a major plasma membrane transporter for iron but also Cd2+. By analysing the incidence of NO scavenging or inhibition of its synthesis during Cd2+ treatment, we demonstrated that NO contributes to Cd2+-triggered inhibition of root growth. To understand the mechanisms underlying this process, a microarray analysis was performed in order to identify NO-modulated root genes up- and down-regulated during Cd2+ treatment. Forty-three genes were identified encoding proteins related to iron homeostasis, proteolysis, nitrogen assimilation/metabolism and root growth. These genes include IRT1. Investigation of the metal and ion contents in Cd2+-treated roots in which NO synthesis was impaired indicates that IRT1 up-regulation by NO was consistently correlated to NO ability to promote Cd2+ accumulation in roots. This analysis also highlights that NO is responsible for Cd2+-induced inhibition of root Ca2+ accumulation. Taken together, our results suggest that NO contributes to Cd2+ toxicity by favouring Cd2+ versus Ca2+ uptake and by initiating a cellular pathway resembling those activated upon iron deprivation.
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