Abstract
In Arabidopsis thaliana, root high-affinity nitrate (NO3-) uptake depends mainly on NRT2.1, 2.4 and 2.5, which are repressed by high NO3- supply at the transcript level. For NRT2.1, this regulation is due to the action of (i) feedback downregulation by N metabolites and (ii) repression by NO3- itself mediated by the transceptor NRT1.1(NPF6.3). However, for NRT2.4 and NRT2.5 the signaling pathway(s) remain unknown along with the molecular elements involved. Here we show that unlike NRT2.1, NRT2.4 and NRT2.5 are not induced in a NO3- reductase mutant but are strongly upregulated following replacement of NO3- by ammonium (NH4+) as the N source. Moreover, increasing NO3- concentration in a mixed nutrient solution with constant NH4+ concentration results in a gradual repression of NRT2.4 and NRT2.5, which is suppressed in a nrt1.1 mutant. This indicates that NRT2.4 and NRT2.5 are subjected to repression by NRT1.1-mediated NO3- sensing, and not to feedback repression by reduced N metabolites. We further show that key regulators of NRT2s transporters, such as HHO1, HRS1, PP2C, LBD39, BT1 and BT2, are also regulated by NRT1.1-mediated NO3-