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Infection and Immunity, September 2008, p. 4009-4018, Vol. 76, No. 9
0019-9567/08/$08.00+0     doi:10.1128/IAI.00027-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Borrelia burgdorferi vlsE Antigenic Variation Is Not Mediated by RecA {triangledown}

Dionysios Liveris,1* Vishwaroop Mulay,2 Sabina Sandigursky,1 and Ira Schwartz1,2

Department of Microbiology & Immunology,1 Department of Biochemistry & Molecular Biology, New York Medical College, Valhalla, New York 105952

Received 8 January 2008/ Returned for modification 2 April 2008/ Accepted 27 June 2008

RecA is a key protein linking genetic recombination to DNA replication and repair in bacteria. Previous functional characterization of Borrelia burgdorferi RecA indicated that the protein is mainly involved in genetic recombination rather than DNA repair. Genetic recombination may play a role in B. burgdorferi persistence by generation of antigenic variation. We report here the isolation of a recA null mutant in an infectious B. burgdorferi strain. Comparison of the in vitro growth characteristics of the mutant with those of the wild-type strain under various conditions showed no significant differences. While the RecA mutant was moderately more sensitive to UV irradiation and mitomycin C than the wild-type strain, the lack of RecA abolished allelic exchange in the mutant. Absence of RecA did not affect the ability of the mutant to infect mice. However, the RecA mutant was attenuated for joint infection in competitive-infection assays with the wild-type strain. vlsE sequence variation in mice was observed in both wild-type and RecA mutant spirochetes, indicating that the mechanism of antigenic variation is not homologous genetic 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

{triangledown} Published ahead of print on 7 July 2008.

Editor: V. J. DiRita

Infection and Immunity, September 2008, p. 4009-4018, Vol. 76, No. 9
0019-9567/08/$08.00+0     doi:10.1128/IAI.00027-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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