Abstract:
: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 uvrA(Bbu) 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 uvrA(Bbu). We conclude that uvrA(Bbu) is functional in B. burgdorferi.
journal_name
FEMS Microbiol Lettjournal_title
FEMS microbiology lettersauthors
Sambir M,Ivanova LB,Bryksin AV,Godfrey HP,Cabello FCdoi
10.1111/j.1574-6968.2011.02226.xsubject
Has Abstractpub_date
2011-04-01 00:00:00pages
172-80issue
2eissn
0378-1097issn
1574-6968journal_volume
317pub_type
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