The NAC080-B12D mediated Module Fine-tunes Iron Deficiency Responses by Modulating Mitochondrial ROS Homeostasis in Arabidopsis

Iron (Fe) deficiency restricts plant growth and necessitates precise regulation of Fe homeostasis to sustain agricultural productivity. We identify a regulatory module comprising NAC080, a constitutively expressed transcription factor, and B12D, a mitochondrial Complex I subunit, that governs oscillatory Fe deficiency responses in Arabidopsis. NAC080 directly activates B12D transcription, preserving mitochondrial Complex I function and restricting mitochondrial H2O2 levels to a signaling-competent range. This H2O2 serves as a dual-functional signal, stimulating FIT transcription while promoting FIT degradation, thereby generating rhythmic FIT protein oscillations essential for balanced Fe uptake. Furthermore, Fe2+ itself directly inhibits mitochondrial H2O2 production, completing the feedback loop. The NAC080-B12D module thus integrates mitochondria-to-nucleus signaling into Fe homeostasis, offering targets for improving Fe utilization in calcareous soils and facilitating crop biofortification.