Nucleotide Excision Repair System of Borrelia burgdorferi Is the Sole Pathway Involved in Repair of DNA Damage by UV Light

• Published in: Journal of Bacteriology Vol. 195; no. 10; pp. 2220 - 2231
• Main Authors: Hardy, Pierre-Olivier, Chaconas, George
• Format: Journal Article
• Language: English
• Published: United States American Society for Microbiology 01-05-2013
• Subjects: Bacterial Proteins - genetics; Bacterial Proteins - metabolism; Bacteriology; Borrelia burgdorferi; Borrelia burgdorferi - genetics; Borrelia burgdorferi - metabolism; Borrelia burgdorferi - radiation effects; DNA damage; DNA Damage - genetics; DNA Damage - radiation effects; DNA repair; DNA Repair - genetics; DNA Repair - physiology; Escherichia coli; Genes; Gram-negative bacteria; mice; mutation; pathogenicity; pathogens; Prokaryotes; prokaryotic cells; Signal Transduction - genetics; Signal Transduction - physiology; Signal Transduction - radiation effects; Ultraviolet radiation; Ultraviolet Rays - adverse effects
• ISSN: 0021-9193; 1098-5530; 1067-8832
• DOI: 10.1128/JB.00043-13

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.