A spatially deployable iron redox rheostat tunes root growth under nutritional stress

Root growth must continuously adjust to fluctuating nutrient availability, yet the mechanisms that quantitatively integrate environmental signals into developmental responses remain poorly understood. Distinct nutrient stresses, including ammonium toxicity and phosphate deficiency, inhibit primary root growth through iron-dependent processes, suggesting that iron acts as a central regulatory node. Here, we show that plants use an antagonistic module composed of CYBDOM ferrireductases and LPR ferroxidases to regulate apoplastic iron homeostasis and control root growth in a graded manner. Genetic perturbation of this module demonstrates that root growth inhibition scales quantitatively with iron accumulation, supporting a proportional control mechanism rather than a binary response. Loss of CYBDOM function causes excessive iron accumulation, elevated reactive oxygen species, and impaired meristem activity, whereas increased CYBDOM activity buffers iron deposition and confers resistance to stress. Mechanistically, iron-induced oxidative stress promotes HYP1 expression, which in turn limits further iron accumulation. Transcriptomic analyses distinguish ammonium-specific responses from Fe-associated transcriptional changes enriched in redox buffering and cell-wall remodeling. Finally, we show that this regulatory module is redeployed in distinct tissues under phosphate deficiency, indicating that plants reuse a conserved iron-based mechanism to coordinate growth across environmental contexts. Together, our findings establish genetically controlled Fe accumulation as a key determinant of developmental plasticity under nutrient stress.