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Two anion transporters AtClCa and AtClCe fulfil interconnecting but not redundant roles in nitrate assimilation pathways.

By Dario Monachello, Michèle Allot, Sabrina Oliva, Anne Krapp, Françoise Daniel-Vedele, Hélène Barbier-Brygoo and Geneviève Ephritikhine

Abstract

International audienceIn plants, the knowledge of the molecular identity and functions of anion channels are still very limited, and are almost restricted to the large ChLoride Channel (CLC) family. In Arabidopsis thaliana, some genetic evidence has suggested a role for certain AtCLC protein members in the control of plant nitrate levels. In this context, AtClCa has been demonstrated to be involved in nitrate transport into the vacuole, thereby participating in cell nitrate homeostasis. * In this study, analyses of T-DNA insertion mutants within the AtClCa and AtClCe genes revealed common phenotypic traits: a lower endogenous nitrate content; a higher nitrite content; a reduced nitrate influx into the root; and a decreased expression of several genes encoding nitrate transporters. * This set of nitrate-related phenotypes, displayed by clca and clce mutant plants, showed interconnecting roles of AtClCa and AtClCe in nitrate homeostasis involving two different endocellular membranes. * In addition, it revealed cross-talk between two nitrate transporter families participating in nitrate assimilation pathways. The contribution to nitrate homeostasis at the cellular level of members of these different families is discussed

Topics: MESH : Anion Transport Proteins, MESH : Arabidopsis, MESH : Nitrates, MESH : Nitrites, MESH : Phenotype, MESH : Receptor Cross-Talk, MESH : Signal Transduction, MESH : Vacuoles, MESH : Arabidopsis Proteins, MESH : Chloride Channels, MESH : DNA, Bacterial, MESH : Genes, Plant, MESH : Intracellular Membranes, MESH : Ion Transport, MESH : Metabolic Networks and Pathways, MESH : Mutation, [ SDV.BV ] Life Sciences [q-bio]/Vegetal Biology
Publisher: Wiley
Year: 2009
DOI identifier: 10.1111/j.1469-8137.2009.02837.x
OAI identifier: oai:HAL:hal-00855498v1
Provided by: Hal-Diderot
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