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Research Paper |
School of Biological Sciences, University of East Anglia, Norwich NR4 7TJ, UK1
Department of Molecular Microbiology, John Innes Centre, Norwich Research Park, Colney Lane, Norwich NR4 7UH, UK2
Department of Animal and Microbial Sciences, University of Reading, Reading RG6 6AJ, UK3
Author for correspondence: Andrew W. B. Johnston. Tel: +44 1603 592264. Fax: +44 1603 592250. e-mail: a.johnston{at}uea.ac.uk
Mutations in a Rhizobium leguminosarum gene, rirA (rhizobial iron regulator), caused high-level, constitutive expression of at least eight operons whose transcription is normally Fe-responsive and whose products are involved in the synthesis or uptake of siderophores, or in the uptake of haem or of other iron sources. Close homologues of RirA exist in other rhizobia and in the pathogen Brucella; many other bacteria have deduced proteins with more limited sequence similarity. None of these homologues had been implicated in Fe-mediated gene regulation. Transcription of rirA itself is about twofold higher in cells grown in Fe-replete than in Fe-deficient growth media. Mutations in rirA reduced growth rates in Fe-replete and -depleted medium, but did not appear to affect symbiotic N2 fixation.
Keywords: iron-mediated regulation, rhizobia, RirA, siderophores
Abbreviations: CAS, chrome azural sulphonate; VB, vicibactin
The GenBank accession number for the RirA sequence is CAC35510.
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