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Published on September 22, 2006; 10.1104/pp.106.087510

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Received July 27, 2006
Accepted September 8, 2006

Regulation of the High-affinity NO3- Uptake System by a NRT1.1-mediated "NO3--demand" Signalling in Arabidopsis

Gabriel Krouk , Pascal Tillard , and Alain Gojon *

Biochimie et Physiologie Moléculaire des Plantes, UMR 5004, Agro-M/CNRS/INRA/UM2, Place Viala, 34060 Montpellier Cedex 1, France

* Corresponding author; email: gojon{at}ensam.inra.fr.

The NRT2.1 gene of Arabidopsis thaliana encodes a major component of the root high-affinity NO3- transport system (HATS) that plays a crucial role in NO3- uptake by the plant. Although NRT2.1 was known to be induced by NO3- and feedback-repressed by reduced N metabolites, NRT2.1 is surprisingly up-regulated when NO3- concentration decreases to a low level (<0.5 mM) in media containing a high concentration of NH4+ or glutamine (≥1 mM). The NRT3.1 gene, encoding another key component of the HATS, displays the same response pattern. This revealed that both NRT2.1 and NRT3.1 are co-ordinately down-regulated by high external NO3- availability, through a mechanism independent from that involving N metabolites. We show here that repression of both genes by high NO3- is specifically mediated by the NRT1.1 NO3- transporter. This mechanism warrants that either NRT1.1 or NRT2.1 is active in taking up NO3- in presence of a reduced N source. Under low NO3-/high NH4+ provision, the NRT1.1-mediated repression of NRT2.1/NRT3.1 is relieved, which allows reactivation of the HATS. The analysis of atnrt2.1 mutants showed that this constitutes a crucial adaptive response against NH4+ toxicity, since NO3- taken up by the HATS in this situation prevents the detrimental effects of pure NH4+ nutrition. It is thus hypothesized that the NRT1.1-mediated regulation of NRT2.1/NRT3.1 is a mechanism aiming to satisfy a specific "NO3- demand" of the plant, in relation with the various specific roles that NO3- plays, in addition of being a N source. A new model is proposed for regulation of the HATS, involving both feed-back repression by N metabolites and NRT1.1-mediated repression by high NO3-.




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