Figure 1.

Summary of early responses in nitrate signaling and assimilation. NO₃⁻ signaling pathway switches its affinity via phosphorylation (modified from Undurraga [41]). Nitrate-responsive genes are depicted in light green, transcription factors in purple, and microRNAs in grey. For clarity purposes, the cell nucleus is shown. Phosphatidylinositol-specific (PI-PLC) and Ca²⁺-dependent pathways. At Low NO₃⁻ condition, protein kinases CBL1/9–CIPK23 complex phosphorylates NRT1.1 and changes it into a high-affinity transporter, which activates PLC and results in calcium influx (Ca²⁺ acts as a second messenger). This cascade mediates changes in the expression of transcription factors (TGA1/4 *) and genes involved in nitrate transport (NRT2.1, NRT2.2, and NRT3.1) and nitrate assimilation (NIA1 and NiR). Nonphosphorylated form of NRT1.1-induced signaling. Nitrate-induced Ca²⁺-ANR1 signaling that promotes lateral root (LR) initiation is assumed to be a nonphosphorylated form of NRT1.1 signaling after the supply of nitrate in limited-nitrate conditions. (C) PI-PLC and Ca²⁺-independent pathways. Conversely, AFB3 is regulated by nitrate in a phospholipase C (PLC)- and calcium-independent manner. ABF3 modulates the expression of NAC4 and OBP4 with subsequent effects on root remodeling. Finally, nitrate assimilation produces organic N, which induces miR393 and represses miR167 (grey) and regulates the abundance of AFB3 and ARF8, respectively. * TGA1 and TGA4 are redundant regulatory factors that mediate nitrate responses in Arabidopsis roots. However, the interaction between TGA4 and the PLC–calcium pathway has not been experimentally validated.