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Fec system includes genes involved in regulation and expression of E. coli iron transporters. fecABCDE genes express the ferric citrate transporter when bacteria iron status is low or deficient. The induction of genes fecABCDE integrates a signaling cascade that begins at the cell surface and is extended to the cytoplasm. To do this, three specific proteins are involved : FecA in outer membrane, FecR in cytoplasmic membrane and FecI in cytoplasm. This module FecA-FecR-FecI is known as a signal transduction system between three compartments (outside, periplasm and cytoplasm).

The signaling pathway begins when the outer membrane receptor FecA binds to its ligand, ferric dicitrate. This binding causes structural changes in FecA that allow the interaction of its amino terminal end to the carboxy terminal end of FecR in the periplasm. FecR, a transmembrane protein, transmits the signal to the cytoplasm, where it activates FecI. FecI is an extracitoplasmatic function (ECF) sigma factor that, when activated, binds to core RNA polymerase and directs the complex to the upstream promoter of fecABCDE transport genes to initiate transcription, this is PfecA.

In addition, the transcription of regulatory genes fecIR is controlled by the internal iron status through the Fur repressor. When the Fur protein is loaded with Fe 2+, it represses fecIR transcription and prevents the fec gene expression. Therefore, the fec transport gene transcription is subjected to a double control: first, cells detect iron deficiency. Then, regulatory proteins FecI and FecR are synthesized, which, if ferric citrate is available, initiate the transcription of fec transport genes.

Dicitrate ferric transport through the outer membrane requires an energy transduction complex consisting of TonB, ExbB and Exb cytoplasmic membrane proteins.

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