Résumé
Potassium (K+) starvation induces the expression of gene HAK5 encoding a high-affinity K+ uptake protein, but how plants perceive the K+ status and the signaling intermediaries involved in the response remains largely unknown. To identify key regulators of K+ nutrition in Arabidopsis, a genetic screen was performed using an pHAK5:LUC reporter line, and a mutant showing stable induction of the reporter under K+-sufficient conditions was isolated. Mapping-by-sequencing identified two linked mutations affecting genes involved in K+ and nitrate nutrition, namely a loss-of-function in the K+ uptake channel AKT1 and a gain-of-function allele of the nitrate transporter NPF6.2/NRT1.4 (NPF6.2V210M) that doubled the rate of nitrate transport. We report that the physical interaction of NPF6.2 and HAK5 transport proteins resulted in reciprocal interference. Co-expression in Xenopus oocytes of NPF6.2 with the regulatory kinase CIPK23 or the mutant protein NPF6.2V210M alone inhibited HAK5 transport, whereas HAK5 inhibited nitrate transport by NPF6.2 and NPF6.2V210M. We conclude that mutation NPF6.2V210M enhanced the nutritional defects associated to the loss of AKT1 function through the inhibition of HAK5. These findings evidence an intimate molecular crosstalk between transporters involved in the mineral nutrition of plants. The mutual interference when both transport systems are operative may represent a novel integrative regulatory mechanism in mineral nutrition.