Résumé
Iron (Fe) homeostasis is crucial for all living organisms. Perturbations of Fe uptake, transport, metabolism or storage are responsible of neurodegenerative diseases and cancer in humans, and alter productivity and product quality of plants. In mammals, an integrated post-transcriptional mechanism couples the regulation of both Fe deficiency and excess responses. Whether an integrated pathway involving common players controls these responses in plants is still to be determined. Using a combination of molecular, genetic and biochemical approaches, we found that bHLH105/ILR3, a transcriptional activator of Arabidopsis responses to Fe shortage negatively regulates ferritin genes expression, the main markers of the plant responses to Fe excess. We demonstrated that various facets of plant development in response to Fe deficiency or excess rely on ILR3. We thus showed that ILR3 repressed the expression of several structural genes involved in the control of Fe homeostasis through its dimerization with bHLH47/PYE. Genome wide identification of ILR3 DNA targets (ChIP-seq) highlighted the preponderant role that ILR3 plays in the control of Fe homeostasis in Arabidopsis. Altogether, we found that ILR3 is at the centre of the transcriptional regulatory network that controls Fe homeostasis in Arabidopsis, where it acts as both transcriptional activator and repressor.