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Journal of Bacteriology, April 2004, p. 2275-2280, Vol. 186, No. 8
0021-9193/04/$08.00+0     DOI: 10.1128/JB.186.8.2275-2280.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Functional Properties of Borrelia burgdorferi recA

Dionysios Liveris,1* Vishwaroop Mulay,1,2 and Ira Schwartz1,2,3

Department of Microbiology & Immunology,1 Department of Biochemistry & Molecular Biology,2 Department of Medicine, New York Medical College, Valhalla, New York 105953

Received 18 August 2003/ Accepted 15 December 2003

Functions of the Borrelia burgdorferi RecA protein were investigated in Escherichia coli recA null mutants. Complementation with B. burgdorferi recA increased survival of E. coli recA mutants by 3 orders of magnitude at a UV dose of 2,000 µJ/cm2. The viability at this UV dose was about 10% that provided by the homologous recA gene. Expression of B. burgdorferi recA resulted in survival of E. coli at levels of mitomycin C that were lethal to noncomplemented hosts. B. burgdorferi RecA was as effective as E. coli RecA in mediating homologous recombination in E. coli. Furthermore, E. coli {lambda} phage lysogens complemented with B. burgdorferi recA produced phage even in the absence of UV irradiation. The level of phage induction was 55-fold higher than the level in cells complemented with the homologous recA gene, suggesting that B. burgdorferi RecA may possess an enhanced coprotease activity. This study indicates that B. burgdorferi RecA mediates the same functions in E. coli as the homologous E. coli protein mediates. However, the rapid loss of viability and the absence of induction in recA expression after UV irradiation in B. burgdorferi suggest that recA is not involved in the repair of UV-induced damage in B. burgdorferi. The primary role of RecA in B. burgdorferi is likely to be a role in some aspect of recombination.


* Corresponding author. Mailing address: Department of Microbiology & Immunology, New York Medical College, Valhalla, NY 10595. Phone: (914) 594-4658. Fax: (914) 594-4176. E-mail: dionysios_liveris{at}nymc.edu.


Journal of Bacteriology, April 2004, p. 2275-2280, Vol. 186, No. 8
0021-9193/04/$08.00+0     DOI: 10.1128/JB.186.8.2275-2280.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • Liveris, D., Mulay, V., Sandigursky, S., Schwartz, I. (2008). Borrelia burgdorferi vlsE Antigenic Variation Is Not Mediated by RecA. Infect. Immun. 76: 4009-4018 [Abstract] [Full Text]  
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  • Eggers, C. H., Caimano, M. J., Radolf, J. D. (2004). Analysis of Promoter Elements Involved in the Transcriptional Initiation of RpoS-Dependent Borrelia burgdorferi Genes. J. Bacteriol. 186: 7390-7402 [Abstract] [Full Text]