IAI Accepts, published online ahead of print on 26 October 2009

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Infect. Immun. doi:10.1128/IAI.01018-09
Copyright (c) 2009, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Characterization of a Conditional bosR Mutant in Borrelia burgdorferi

Jenny A. Hyde, Dana K. Shaw, Roger Smith III, Jerome P. Trzeciakowski, and Jon T. Skare^*

Department of Microbial and Molecular Pathogenesis and Systems Biology and Translational Medicine, College of Medicine, Texas A&M Health Science Center, College Station, Texas 77843-1114; Department of Veterinary Pathobiology, College of Veterinary Medicine, Texas A&M University, College Station, Texas 77843-4467

^* To whom correspondence should be addressed. Email: jskare{at}medicine.tamhsc.edu.

Borrelia burgdorferi, the etiological agent of Lyme disease, adapts to unique host environments as a consequence of its complex lifecycle that spans both arthropod and mammalian species. In this regard B. burgdorferi must adapt to varying environmental signals, pH, temperature, O₂ and CO₂ levels, to establish an infectious foci. We hypothesize that the BosR protein functions as a global regulator that is required for both borrelial oxidative homeostasis and pathogenesis. To assess the role of BosR on B. burgdorferi, we constructed an IPTG regulated bosR strain. The selective decrease of bosR resulted in a change in growth when cells were cultured either anaerobically or microaerobically; however, a distinct growth defect was observed for anaerobically grown B. burgdorferi relative to the growth attenuation observed for microaerobically grown B. burgdorferi. B. burgdorferi cells to which BosR levels were reduced were more sensitive to hydrogen peroxide and produced lower levels of NapA (Dps) and SodA, proteins involved in the oxidative stress response. In addition, the levels of OspC and DbpA were also induced coincident with increased BosR levels, suggesting that BosR interfaces with the RpoS regulatory cascade, which is known to modulate virulence gene expression in B. burgdorferi. Taken together, these results indicate that BosR is involved in the resistance of B. burgdorferi to oxidative stressors and affects the expression of genes, either directly or indirectly, whose products are important in borrelial pathogenesis.