Iron (Fe) transport and utilization are controlled by Fe-dependent transcriptional cascades. Many genes participate in these processes, transcriptionally controlled by Fe-status. Thorough knowledge of the translational check-points is lacking. We identified a non-response to Fe-deficiency1-1 (nrf1-1) mutant of Arabidopsis thaliana, which displayed a hypersensitive phenotype under Fe-deficient conditions. By mapping nrf1-1, we found that the AT3G13440 locus encoding a HemK methyltransferase is responsible for the phenotype. Analyses of ProUBQ10:NRF1CDS overexpression nrf1-1 lines and a T-DNA insertion mutant nrf1-2, confirmed that loss-of-function of NRF1 results in enhanced Fe-starvation-sensitivity. NRF1 is required for the proper expression of the majority of Fe-deficiency-inducible (FDI) genes. The nrf1 mutants accumulated more polysomes in the roots, due to stalled ribosomes on several transcripts. Ribosome-footprint (RF) mapping revealed that ribosomes are stalled at a stop codon that amplified the stalling of trailing ribosomes. We detected higher RF levels in many FDI transcripts in nrf1-2. Our study demonstrates the requirement of NRF1 for an accurate termination of protein synthesis essential not only for a precise iron homeostasis, but also cellular ion balance. NRF1 is also important for normal growth and development. A check-point that fine-tunes peptide release in plants is uncovered.
