Nitrate-dependent control of shoot K homeostasis by NPF7.3/NRT1.5 and SKOR in Arabidopsis

Abstract

Root-to-shoot translocation and shoot homeostasis of potassium (K) determine nutrient balance, growth and stress tolerance of vascular plants. To maintain the cation-anion balance, xylem loading of K+ in the roots relies on the concomitant loading of counter-anions like nitrate (NO3-). However, the co-regulation of these loading steps is unclear. Here, we show that the bi-directional, low-affinity NO3- transporter NPF7.3/NRT1.5 is important for the NO3--dependent K+ translocation in Arabidopsis thaliana. Lack of NPF7.3/NRT1.5 resulted in K deficiency in shoots under low NO3- nutrition, while the root elemental composition was unchanged. Gene expression data corroborated K deficiency in the nrt1.5-5 shoot, while the root responded with a differential expression of genes involved in cation-anion balance. A grafting experiment confirmed that the presence of NPF7.3/NRT1.5 in the root is a prerequisite for proper root-to-shoot translocation of K+ under low NO3- supply. Since the depolarization-activated K+ channel SKOR has previously been described as a major contributor for root-to-shoot translocation of K+ in Arabidopsis, we addressed the hypothesis that NPF7.3/NRT1.5-mediated NO3- translocation might affect xylem loading and root-to-shoot K+ translocation via SKOR. Indeed, growth of nrt1.5-5 and skor-2 single and double mutants under different K/NO3- regimes revealed that both proteins contribute to K+ translocation from root to shoot. SKOR activity dominates under high NO3- and low K+ supply, whereas NPF7.3/NRT1.5 is required under low NO3- availability. This study unravels nutritional conditions as a critical factor for the joint activity of SKOR and NPF7.3/NRT1.5 for shoot K homeostasis.