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Arch Microbiol. 1997 Jun;167(6):325-31.

Surface signaling: novel transcription initiation mechanism starting from the cell surface.

Author information

  • Mikrobiologie / Membranphysiologie, Universität Tübingen, Auf der Morgenstelle 28, D-72076 Tübingen, Germany. vbraun@uni-tuebingen.de

Abstract

Transcription of the ferric citrate transport genes of Escherichia coli is induced by a novel mechanism. Ferric citrate, the inducer, does not have to enter the cytoplasm to initiate transcription. Interaction of ferric citrate with the outer membrane receptor protein FecA induces transcription of the fec transport gene operon consisting of the fecIRABCDE genes. A signal from FecA occupied with ferric citrate is transmitted across the outer membrane into the periplasm with the help of the electrochemical potential of the cytoplasmic membrane and the Ton system. The signal is then transduced across the cytoplasmic membrane by the FecR protein, which in turn activates the FecI sigma-factor that directs the RNA polymerase core-enzyme to the fec transport gene promoter. The promoter of the regulatory genes fecI and fecR is not controlled by ferric citrate but is regulated by iron via the Fur repressor. It is proposed that the information flux from the cell surface to the cytoplasm involves a series of conformational changes of the proteins FecA, FecR, and FecI in that order. The level of the regulatory proteins FecI and FecR is adjusted to the intracellular iron concentration and determines the degree of the response of the cell to ferric citrate in the medium. Ferric citrate induces transcription of the fec transport genes under iron-limiting conditions. A regulatory device similar to the ferric citrate transport system exists in Pseudomonas putida WCS358. The synthesis of the outer membrane receptor PupB, involved in the transport of the ferric pseudobactins BN7 and BN8, is induced by the ferric siderophores and requires PupB and two proteins homologous to FecI and FecR.

PMID:
9148773
[PubMed - indexed for MEDLINE]
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