Nitrate sensing through NLP7-NIGT1.3 regulates iron deficiency responses and growth trade-offs in Arabidopsis.

Nitrate fertilizers exacerbate Fe deficiency in plants, a phenomenon traditionally attributed to rhizosphere alkalinization that reduces Fe bioavailability. However, whether nitrate itself acts as a signaling molecule in this process has remained unclear. Here, we demonstrate that nitrate functions as an essential signaling molecule that regulates Fe deficiency responses in Arabidopsis through NLP7, a central nitrate sensor. Nitrate deficiency, but not ammonium deficiency, abolishes Fe deficiency-induced chlorosis and suppresses the expression of Fe uptake genes (IRT1, FIT), confirming nitrate's specific signaling role. We show that Fe deficiency triggers rapid nuclear accumulation of NLP7 in a strictly nitrate-dependent manner. Loss-of-function nlp7 mutants exhibit attenuated Fe deficiency responses, including reduced FCR activity and diminished induction of IRT1, FRO2, and FIT, yet exhibit reduced chlorosis under Fe deficiency, indicating alleviation of stress symptoms rather than genuine enhancement of Fe tolerance. Transcriptome and molecular analyses identify NIGT1.3 as a direct transcriptional target of NLP7; NIGT1.3 in turn represses NRT1.1 transcription, establishing a regulatory cascade from nitrate sensing to Fe homeostasis modulation. Notably, growth-chlorophyll correlation analysis reveals that plant growth positively correlates with chlorophyll content under Fe sufficiency but negatively correlates under Fe deficiency, uncovering a growth-stress trade-off mediated by the NLP7-NIGT1.3 module. Collectively, our findings establish NLP7 as a central hub integrating nitrate signaling with Fe deficiency responses and reveal a regulatory mechanism that balances stress adaptation with growth maintenance under combined nitrate and Fe nutritional stress.