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

The accumulation of NH 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 (NH) 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 NH plays a pivotal role when Arabidopsis thaliana plants are subject to Fe deficiency. The Arabidopsis amt1-3 mutant, which is defective in endogenous NH sensing, exhibited increased sensitivity to Fe deficiency compared to WT (wild type; Col-0). In addition, exogenous application of NH significantly alleviated Fe deficiency symptoms in plants. NH 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. NH 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, NH 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.