Repair of cross-linked DNA and survival of Escherichia coli treated with psoralen and light: effects of mutations influencing genetic recombination and DNA metabolism

Sinden, Richard R.; Cole, Ronald S.

doi:10.1128/jb.136.2.538-547.1978

Cited by 97 publications

(23 citation statements)

References 46 publications

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“…, 1976;Poll et al, 1984;Zolan et al, 1982b;Sancar et al, 1986) indicates that an effective repair system for crosslinks must exist. While a number of possible mechanisms have been proposed, the actual mechanism has not been elucidated (Sinden and Cole, 1978;Saffran and Cantor, 1984;Cole, 1973). Of course prokaryotic and eukaryotic systems may utilise different mechanisms for dealing with crosslinks and other bifilar damage in their DNA Each of the furocoumarins produces a slightly different spectrum of photoproducts.…”

Section: Introductionmentioning

confidence: 99%

Photoadducts of 8‐methoxypsoralen to Cytosine in Dna

Calvin

Hanawalt

1987

Photochem & Photobiology

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Abstract— The isolation and partial characterization of several photoadducts formed between 8‐methoxypsoralen (8‐MOP) and cytosine is described. The formation of these adducts was analysed in E. coli DNA containing 3H‐labeled cytosine and/or 14C‐labeled thymine, and in oligonucleotides of defined sequence. The major initial adduct has been identified as an 8‐MOP cytosine monoadduct, most likely forming at the pyrone end of the 8‐MOP molecule. Further irradiation converts this adduct to several other species, including both cytosine:cytosine and cytosine:thymine diadducts, as well as a number of derivative monoadducts. One isomer of the C:T diadduct appears to undergo a reversible isomerization under the conditions normally used to analyse adduct mixtures by HPLC. The isomerization can cause this adduct to exhibit a retention time on reversed‐phase HPLC closely resembling either that of a thymine‐thymine crosslink or a thymine monoadduct.

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Section: Introductionmentioning

confidence: 99%

Photoadducts of 8‐methoxypsoralen to Cytosine in Dna

Calvin

Hanawalt

1987

Photochem & Photobiology

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“…Therefore, E. coli exposed to MMC needs recombination to repair damage done by MMC. It has been reported that in contrast to eukaryotes, E. coli lacks a mechanism to inhibit chromosomal replication when its DNA is damaged (Sinden and Cole 1978;Kuzminov 1999). In addition, DNA replication in E. coli is often the limiting step in their cell cycle (Bremer and Dennis 1996) while eukaryotes can easily cope with a replication delay, as their S phase is only a fraction of their overall cell cycle (Bremer and Dennis 1996).…”

Section: Discussionmentioning

confidence: 99%

Acclimation and repair of DNA damage in recombinant bioluminescent Escherichia coli

Min

2003

J Appl Microbiol

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Aims: The aim of this study is to understand different adaptive responses in bacteria caused by three different mutagens, namely, an intercalating agent, an alkylating agent and a hydroxylating agent, and the repair systems according to the type of DNA damage, that is, DNA cross-linking and delayed DNA synthesis, alkylation and hydroxylation of DNA. A recombinant bioluminescent Escherichia coli, DPD2794 with the recA promoter fused to luxCDABE originating from Vibrio fischeri, was used in this study. Methods and Results: The recombinant bioluminescent E. coli strain DPD2794, containing a recA promoter fused to luxCDABE from V. fischeri, was used to detect adaptive and repair responses to DNA damage caused by mitomycin C (MMC), and these responses were compared with those when the cells were induced with N-methyl-N-nitro-N-nitrosoguanidine (MNNG) and hydrogen peroxide (H 2 O 2 ). The response ratio between the induced samples and that of the controls decreased suddenly when the induced culture was used in further inductions, indicating a possible adaptive response to DNA damage. DNA damage, or the proteins produced, because of MMC addition does not appear to be completely resolved until the seventh sub-culture after the initial induction, whereas simple damage, such as the base modification caused by MNNG and H 2 O 2 , appears to be repaired rapidly as evidenced by the quick recovery of sensitivity. Conclusions: These results suggest that it takes more time to completely repair DNA damage caused by MMC, as compared with a simple repair such as that required for the damage caused by MNNG and H 2 O 2 . Therefore, repair of the damage caused by these three mutagens is controlled by different regulons, even though they all induced the recA promoter. Significance and Impact of the Study: Using a bioluminescent E. coli harbouring a recA promoter-lux fusion, it was found that different adaptive responses and repair systems for DNA damage caused by several mutagens exists in E. coli.

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“…Because our screening involved enhanced cell killing on mitomycin‐containing plates, the question arises whether a decreased mutagenic bypass could also contribute to host mitomycin sensitivity. Mitomycin C is known to induce mostly interstrand cross‐links that are primarily repaired by recombination (Iyer and Szybalski, 1963; Sinden and Cole, 1978). Accordingly, bacteria expressing no (or inactive) UmuD′C complex have a wild‐type mitomycin sensitivity (Attfield and Pinney, 1984; unpublished data).…”

Section: Discussionmentioning

confidence: 99%

Specific amino acid changes enhance the anti‐recombination activity of the UmuD′C complex

Sommer

Coste

Bailone

2000

Molecular Microbiology

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In addition to being an essential component of trans‐lesion synthesis, the UmuD′C complex is an antagonist of RecA‐mediated homologous recombination. When constitutively expressed at an elevated concentration, the UmuD′C complex sensitizes recA+ bacteria to DNA damage, whereas it has no effect on bacteria expressing a RecA [UmuR] protein that overcomes recombination inhibition. Using as a genetic screen enhanced cell killing on mitomycin plates, we isolated novel umuD′ and umuC mutations that restored mitomycin sensitivity to recA D112G [UmuR] bacteria overproducing the UmuD′C complex. The mutations were named [Rin++] because a characterization in a recA+ as well in a recA D112G background showed that they enhanced UmuD′C‐promoted recombination inhibition in two assays, conjugational recombination and recombinational repair of palindrome‐containing DNA. The [Rin++] mutations affect five amino acids, G25D, S28T, P29L, E35K, and T95R, in UmuD′ and seven, F10L, Y270C, K277E, F287L, F287S, K342Q and F351I, in UmuC. These amino acids might play a key role in the UmuD′C anti‐recombination activity. None of the [Rin++] mutations enhanced UmuD′C‐promoted mutagenic bypass of UV lesions, in contrast, several lead to a defect in this process. In this study, we discuss a few molecular mechanisms that could account for the recombination and mutagenesis phenotypes of a mutant UmuD′C [Rin++] complex.

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Repair of cross-linked DNA and survival of Escherichia coli treated with psoralen and light: effects of mutations influencing genetic recombination and DNA metabolism

Cited by 97 publications

References 46 publications

Photoadducts of 8‐methoxypsoralen to Cytosine in Dna

Photoadducts of 8‐methoxypsoralen to Cytosine in Dna

Acclimation and repair of DNA damage in recombinant bioluminescent Escherichia coli

Specific amino acid changes enhance the anti‐recombination activity of the UmuD′C complex

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