The uvrB gene of Pseudomonas aeruginosa is not DNA damage inducible

Rivera, Eusebi; Vila, Laura; Barbé, Jordi

doi:10.1128/jb.178.18.5550-5554.1996

Cited by 19 publications

(12 citation statements)

References 24 publications

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“…For example, in E. coli expression of the uvrA, uvrB, and uvrD genes is significantly induced following DNA damage. However, in P. aeruginosa, an organism that is more sensitive to UVC than E. coli, both uvrA and uvrB are not DNA damage inducible, although this bacterium possesses an SOSlike system (38,39). In MR-1, we observed strong SOS induction following UVB or UVC exposure, which included increases in transcript levels of lexA and recA as well as the umuDC operon (unpublished data).…”

Section: Discussionmentioning

confidence: 81%

Survival of Shewanella oneidensis MR-1 after UV Radiation Exposure

Qiu

Sundin

Chai

et al. 2004

Appl Environ Microbiol

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؊2 , respectively. Photoreactivation conferred an increased survival rate to MR-1 of as much as 177-to 365-fold, 11-to 23-fold, and 3-to 10-fold following UVC, UVB, and solar light irradiation, respectively. A significant UV mutability to rifampin resistance was detected in both UVC-and UVB-treated samples, with the mutation frequency in the range of 10 ؊5 to 10 ؊6 . Unlike in E. coli, the expression levels of the nucleotide excision repair (NER) component genes uvrA, uvrB, and uvrD were not damage inducible in MR-1. Complementation of Pseudomonas aeruginosa UA11079 (uvrA deficient) with uvrA of MR-1 increased the UVC survival of this strain by more than 3 orders of magnitude. Loss of damage inducibility of the NER system appears to contribute to the high sensitivity of this bacterium to UVR as well as to other DNA-damaging agents.

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Section: Discussionmentioning

confidence: 81%

Survival of Shewanella oneidensis MR-1 after UV Radiation Exposure

Qiu

Sundin

Chai

et al. 2004

Appl Environ Microbiol

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“…The possibility of a NER mechanism, which is also known to repair similar lesions, was raised because enzymatic removal of 8-oxo-G in P. gingivalis occurred by DNA cleavage several bases away from the lesion (27). Similar to the case in other organisms (40,51), uvrB in P. gingivalis appears to play the expected role, as the uvrB-defective mutant was more sensitive to UV irradiation than the wild-type strain. There was, however, no difference in sensitivity to oxidative stress in the uvrB-defective mutant (FLL144) compared to the wild type, suggesting that UvrB is not involved in oxidative stress resistance in P. gingivalis.…”

Section: Discussionmentioning

confidence: 99%

DNA Repair of 8-Oxo-7,8-Dihydroguanine Lesions in Porphyromonas gingivalis

Henry¹,

Sandberg

Zhang

et al. 2008

J Bacteriol

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The persistence of Porphyromonas gingivalis in the inflammatory environment of the periodontal pocket requires an ability to overcome oxidative stress. DNA damage is a major consequence of oxidative stress. Unlike the case for other organisms, our previous report suggests a role for a non-base excision repair mechanism for the removal of 8-oxo-7,8-dihydroguanine (8-oxo-G) in P. gingivalis. Because the uvrB gene is known to be important in nucleotide excision repair, the role of this gene in the repair of oxidative stressinduced DNA damage was investigated. A 3.1-kb fragment containing the uvrB gene was PCR amplified from the chromosomal DNA of P. gingivalis W83. This gene was insertionally inactivated using the ermF-ermAM antibiotic cassette and used to create a uvrB-deficient mutant by allelic exchange. When plated on brucella blood agar, the mutant strain, designated P. gingivalis FLL144, was similar in black pigmentation and beta-hemolysis to the parent strain. In addition, P. gingivalis FLL144 demonstrated no significant difference in growth rate, proteolytic activity, or sensitivity to hydrogen peroxide from that of the parent strain. However, in contrast to the wild type, P. gingivalis FLL144 was significantly sensitive to UV irradiation. The enzymatic removal of 8-oxo-G from duplex DNA was unaffected by the inactivation of the uvrB gene. DNA affinity fractionation identified unique proteins that preferentially bound to the oligonucleotide fragment carrying the 8-oxo-G lesion. Collectively, these results suggest that the repair of oxidative stress-induced DNA damage involving 8-oxo-G may occur by a still undescribed mechanism in P. gingivalis.

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“…These observations suggest that RecA does not directly regulate transcription of the uvrB, recG, and ruvB homologs in B. cepacia G4. Likewise, the uvrB gene of P. aeruginosa is not DNA damage inducible, nor is an SOS consensus region found upstream of its promoter (37). Although other DNA repair enzymes may be part of the SOS regulon in B. cepacia G4, it is likely that RecA plays a more pivotal role as a recombinase in protecting the cells from TCErelated damage.…”

Section: Discussionmentioning

confidence: 99%

Requirement of DNA Repair Mechanisms for Survival of Burkholderia cepacia G4 upon Degradation of Trichloroethylene

Yeager

Bottomley²,

Arp

2001

Appl Environ Microbiol

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A Tn5-based mutagenesis strategy was used to generate a collection of trichloroethylene (TCE)-sensitive (TCS) mutants in order to identify repair systems or protective mechanisms that shield Burkholderia cepacia G4 from the toxic effects associated with TCE oxidation. Single Tn5 insertion sites were mapped within open reading frames putatively encoding enzymes involved in DNA repair (UvrB, RuvB, RecA, and RecG) in 7 of the 11 TCS strains obtained (4 of the TCS strains had a single Tn5 insertion within a uvrB homolog). The data revealed that the uvrB-disrupted strains were exceptionally susceptible to killing by TCE oxidation, followed by the recA strain, while the ruvB and recG strains were just slightly more sensitive to TCE than the wild type. The uvrB and recA strains were also extremely sensitive to UV light and, to a lesser extent, to exposure to mitomycin C and H 2 O 2 . The data from this study establishes that there is a link between DNA repair and the ability of B. cepacia G4 cells to survive following TCE transformation. A possible role for nucleotide excision repair and recombination repair activities in TCE-damaged cells is discussed.Trichloroethylene (TCE), a suspected human carcinogen (17), has been used extensively as a metal degreaser, fumigant, and solvent for dry cleaning and in other commercial applications. Because of its widespread use and persistence, TCE is one the most commonly detected organic pollutants at hazardous waste sites and in municipal groundwater supplies in the United States (24, 48). Although it has not been demonstrated that microorganisms can utilize TCE as a growth-supporting substrate under aerobic conditions, a number of bacteria are able to degrade TCE cometabolically; in this process nonspecific oxygenases catalyze the initial transformation (1,8,44).The practicality of utilizing bacteria to degrade TCE via aerobic cometabolism has been questioned, however, due to the cytotoxicity that is almost universally associated with this process. Loss of TCE-degradative activity is often observed with whole cells during TCE transformation (34,36,43,45,49), and each of the TCE-degrading enzymes that have been purified to homogeneity and examined to date (toluene dioxygenase, toluene 2-monooxygenase, and soluble methane monooxygenase) exhibits turnover-dependent inactivation upon TCE oxidation (12,22,33). Additionally, TCE degradation can result in injuries that adversely affect more basic cellular functions, such as general respiratory activity and cell viability (4,16,43,49). Although the exact nature of the destructive species remains unknown, it has been proposed that acyl chlorides, generated from hydrolysis or rearrangement of TCE epoxide (monooxygenase-catalyzed reactions) or TCEdioxetane (dioxygenase-catalyzed reactions), cause damage by alkylating various cellular constituents (12,22,33,43,46). Since cellular toxicity can potentially limit the sustainability of TCE biodegradation under aerobic conditions, a concerted effort has been directed towards identifying strains t...

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The uvrB gene of Pseudomonas aeruginosa is not DNA damage inducible

Cited by 19 publications

References 24 publications

Survival of Shewanella oneidensis MR-1 after UV Radiation Exposure

Survival of Shewanella oneidensis MR-1 after UV Radiation Exposure

DNA Repair of 8-Oxo-7,8-Dihydroguanine Lesions in Porphyromonas gingivalis

Requirement of DNA Repair Mechanisms for Survival of Burkholderia cepacia G4 upon Degradation of Trichloroethylene

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