Functional analysis of Borrelia burgdorferi uvrA in DNA damage protection



This article is corrected by:

  1. Errata: Functional analysis of Borrelia burgdorferi uvrA in DNA damage protection Volume 339, Issue 1, 75, Article first published online: 21 December 2012

  • Editor: Reggie Lo

  • Present address: Anton V. Bryksin, Department of Biochemistry, Rollins Research Center, Emory University School of Medicine, 1510 Clifton Road, Atlanta, GA 30322, USA.

Correspondence: Felipe C. Cabello, Department of Microbiology and Immunology, New York Medical College, Basic Science Building, Valhalla, NY 10595, USA Tel.: +1 914 594 4182; fax: +1 914 594 4176; e-mail:


Bacterial pathogens face constant challenges from DNA-damaging agents generated by host phagocytes. Although Borrelia burgdorferi appears to have much fewer DNA repair enzymes than pathogens with larger genomes, it does contain homologues of uvrA and uvrB (subunits A and B of excinuclease ABC). As a first step to exploring the physiologic function of uvrABbu and its possible role in survival in the host in the face of DNA-damaging agents, a partially deleted uvrA mutant was isolated by targeted inactivation. While growth of this mutant was markedly inhibited by UV irradiation, mitomycin C (MMC) and hydrogen peroxide at doses that lacked effect on wild-type B. burgdorferi, its response to pH 6.0–6.8 and reactive nitrogen intermediates was similar to that of the wild-type parental strain. The sensitivity of the inactivation mutant to UV irradiation, MMC and peroxide was complemented by an extrachromosomal copy of uvrABbu. We conclude that uvrABbu is functional in B. burgdorferi.