Ammonium regulates Fe deficiency responses by enhancing nitric oxide signaling in Arabidopsis thaliana.

The accumulation of NH4+ in response to Fe deficiency plays a role not only in the remobilization of Fe from the root cell wall, but also in the transportation of Fe from root to shoot. Ammonium (NH4+) plays an important role in phosphorus-deficiency responses in rice, but its role in responses to Fe deficiency remains unknown. Here, we demonstrate that the accumulation of NH4+ plays a pivotal role when Arabidopsis thaliana plants are subject to Fe deficiency. The Arabidopsis amt1-3 mutant, which is defective in endogenous NH4+ sensing, exhibited increased sensitivity to Fe deficiency compared to WT (wild type; Col-0). In addition, exogenous application of NH4+ significantly alleviated Fe deficiency symptoms in plants. NH4+ triggers the production of nitric oxide (NO), which then induces ferric-chelate reductase (FCR) activity and accelerates the release of Fe from the cell wall, especially hemicellulose, thereby increasing the availability of soluble Fe in roots. NH4+ also increases soluble Fe levels in shoots by upregulating genes involved in Fe translocation, such as FRD3 (FERRIC REDUCTASE DEFECTIVE3) and NAS1 (NICOTIANAMINE SYNTHASE1), hence, alleviating leaf chlorosis. Overall, NH4+ plays an important role in the reutilization of Fe from the cell wall and the redistribution of Fe from root to shoot in Fe-deficient Arabidopsis, a process dependent on NO accumulation.