Todd Jonathan D, Wexler Margaret, Sawers Gary, Yeoman Kay H, Poole Philip S, Johnston Andrew W B
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.
Microbiology (Reading). 2002 Dec;148(Pt 12):4059-4071. doi: 10.1099/00221287-148-12-4059.
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 N(2) fixation.
豆科根瘤菌(Rhizobium leguminosarum)的rirA基因(根瘤菌铁调节因子)发生突变,导致至少八个操纵子的高水平组成型表达,这些操纵子的转录通常对铁有反应,其产物参与铁载体的合成或摄取,或血红素或其他铁源的摄取。RirA的紧密同源物存在于其他根瘤菌和病原体布鲁氏菌中;许多其他细菌也有推导出来的序列相似性更有限的蛋白质。这些同源物均未涉及铁介导的基因调控。在铁充足的生长培养基中生长的细胞中,rirA自身的转录比在缺铁的生长培养基中大约高两倍。rirA突变降低了在铁充足和缺铁培养基中的生长速率,但似乎不影响共生固氮。