1887

Abstract

A gene cluster similar to haem iron uptake loci of bacterial pathogens was identified in . This locus (‘ haem uptake’) consisted of the receptor gene and the operon encoding a typical ABC transporter. Expression of and from mapped transcriptional-start sites occurred under iron-restricted growth conditions and was directly controlled by the Fur protein. Binding of Fur was demonstrated by DNase footprinting of two adjacent ‘Fur boxes’ that overlapped both the and promoters. Two tandem repeats of 154 bp were identified downstream of the operon, each of which contained a strong Fur-dependent promoter driving expression of iron-regulated RNAs antisense to . Mutant strains with deletions in and showed greatly reduced growth with either haem or haemoglobin as the only iron source: the defects were complemented by plasmids harbouring the or the genes, respectively. Deletions of or of the tandem repeats had only minor effects on haem utilization. The remaining haem and haemoglobin uptake still observed in the Δ or Δ deletion mutants was due to a second haem-acquisition system, , which was also under the direct control of Fur. This second haem-receptor gene, , was identified upstream of and in an operon with , encoding a haem-binding extracellular protein. A Δ mutant also exhibited decreased utilization of haem and haemoglobin, and a Δ Δ double mutant was virtually unable to take up either compound. Both the PhuR and HasR proteins were detected in the outer-membrane fraction of grown in low-iron media. Taken together, the evidence suggests that the and loci encode two distinct systems required for the acquisition of haem and haemoglobin in .

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2000-01-01
2024-04-25
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