Affiliation:
1. Departments of Microbiology, Immunology & Infectious Diseases, Snyder Institute for Chronic Diseases, University of Calgary, Calgary, Alberta, Canada
2. Biochemistry & Molecular Biology, Snyder Institute for Chronic Diseases, University of Calgary, Calgary, Alberta, Canada
Abstract
ABSTRACT
To survive and avoid accumulation of mutations caused by DNA damage, the genomes of prokaryotes encode a variety of DNA repair pathways most well characterized in
Escherichia coli
. Some of these are required for the infectivity of various pathogens. In this study, the importance of 25 DNA repair/recombination genes for
Borrelia burgdorferi
survival to UV-induced DNA damage was assessed. In contrast to
E. coli
, where 15 of these genes have an effect on survival of UV irradiation, disruption of recombinational repair, transcription-coupled repair, methyl-directed mismatch correction, and repair of arrested replication fork pathways did not decrease survival of
B. burgdorferi
exposed to UV light. However, the disruption of the
B. burgdorferi
nucleotide excision repair (NER) pathway (
uvrA
,
uvrB
,
uvrC
, and
uvrD
) resulted in a 10- to 1,000-fold increase in sensitivity to UV light. A functional NER pathway was also shown to be required for
B. burgdorferi
resistance to nitrosative damage. Finally, disruption of
uvrA
,
uvrC
, and
uvrD
had only a minor effect upon murine infection by increasing the time required for dissemination.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
Cited by
18 articles.
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