Biological properties of imidazole ring-opened N7-methylguanine in M13mp18 phage DNA

Tudek, Barbara; Boiteux, Serge; Laval, Jacques

doi:10.1093/nar/20.12.3079

Cited by 71 publications

(59 citation statements)

References 43 publications

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“…Thus, replication errors at mFapyG sites emerging in fully replicated DNA will be suppressed to a very low level of ϳ1/10 6 replicated mFapyG lesions based on the ratio of f ins ϫ f ext for insertion of C (3.7 ϫ 10 2 ) versus T (4.0 ϫ 10 Ϫ4 ). This provides a reasonable model and explanation for the lack of (or very low) mutagenicity of mFapyG lesions found in the transfection assays of DMS/ NaOH-treated M13 DNA (19,20), although the DNA polymerase involved in vivo is different from the present study (polymerase III holoenzyme in uninduced E. coli cells and possibly polymerase II, IV, or V in SOS-induced cells) (40,41). Conversely, the replication error frequency at 8-oxoG sites emerging in fully replicated DNA is high (ϳ1/10 replicated 8-oxoG lesions according to the ratio of f ins ϫ f ext for insertion of C (9.5 ϫ 10 2 ) versus A (8.9 ϫ 10)), which has been substantiated by a number of in vivo studies (9,11,(42)(43)(44).…”

Section: Figsupporting

confidence: 51%

Effects of a Guanine-derived Formamidopyrimidine Lesion on DNA Replication

Asagoshi

Terato

Ohyama

et al. 2002

Journal of Biological Chemistry

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2,6-Diamino-4-hydroxy-5-formamidopyrimidine derived from guanine (FapyG) is a major DNA lesion formed by reactive oxygen species. In this study, a defined oligonucleotide template containing a 5-N-methylated analog of FapyG (mFapyG) was prepared, and its effect on DNA replication was quantitatively assessed in vitro. The results were further compared with those obtained for 7,8-dihydro-8-oxoguanine and an apurinic/ apyrimidinic site embedded in the same sequence context. mFapyG constituted a fairly strong but not absolute block to DNA synthesis catalyzed by Escherichia coli DNA polymerase I Klenow fragment with and without an associated 3-5 exonuclease activity, thereby permitting translesion synthesis with a limited efficiency. The efficiency of translesion synthesis was G > 7,8-dihydro-8-oxoguanine > mFapyG > apurinic/apyrimidinic site. Analysis of the nucleotide insertion (f ins ‫؍‬ V max /K m for insertion) and extension (f ext ‫؍‬ V max /K m for extension) efficiencies for mFapyG revealed that the extension step constituted a major kinetic barrier to DNA synthesis. When mFapyG was bypassed, dCMP, a cognate nucleotide, was preferentially inserted opposite the lesion (dCMP (relative f ins ‫؍‬ 1) > > dTMP (2.4 ؋ 10 ؊4 ) Ϸ dAMP (8.1 ؋ 10 ؊5 ) > dGMP (4.5 ؋ 10 ؊7 )), and the primer terminus containing a mFapyG:C pair was most efficiently extended (mFapyG:C (relative f ext ‫؍‬ 1) > mFapyG:T (4.6 ؋ 10 ؊3 ) > > mFapyG:A and mFapyG:G (extension not observed)). Thus, mFapyG is a potentially lethal but not premutagenic lesion.Reactive oxygen species formed by aerobic metabolism, phagocytic blood cells upon inflammation, ionizing radiation, and photosensitized reactions generate structurally diverse oxidative damage to DNA that stores vital genetic information of cells (1-3). Base lesions thus formed are generally restored by the base excision repair pathway involving multiple enzymes such as N-glycosylase/AP 1 lyase, AP endonuclease, DNA polymerase, and DNA ligase (4, 5). However, if left unrepaired, they result in mutations and/or cell death. It has also been implied that oxidative DNA damage is involved in carcinogenesis and various degenerative diseases (6, 7). 7,8-Dihydro-8-oxoguanine (8-oxoG) and 2,6-diamino-4-hydroxy-5-formamidopyrimidine derived from guanine (FapyG) have been identified as major products in the reaction of DNA with reactive oxygen species (Fig. 1A) (1, 2). When formed in DNA, 8-oxoG in a template directs incorporation of non-cognate dAMP as well as cognate dCMP during translesion synthesis by DNA polymerases, thereby inducing GC-to-TA transversions (8, 9). Similarly, when formed in a cellular nucleotide pool, a 2Ј-deoxyribonucleotide form of 8-oxoG can be incorporated opposite adenine as well as cytosine in a DNA template, inducing AT-to-CG transversions (10 -12). Mispair formation between 8-oxoG and adenine leading to mutation involves an unusual syn-conformer of 8-oxoG that can form two hydrogen bonds between O-6 and N-7-H in 8-oxoG and N-6 -H and N-1 in adenine without introducing significan...

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Section: Figsupporting

confidence: 51%

Effects of a Guanine-derived Formamidopyrimidine Lesion on DNA Replication

Asagoshi

Terato

Ohyama

et al. 2002

Journal of Biological Chemistry

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“…Methylated plasmids were subsequently separated from the unreacted MMS by centrifugation through G-50 microcolumns (Pharmacia), and DNA concentrations were determined. Based on previous results (38) and taking into account the size of the DNA molecules and the incubation time and temperature, we calculated the methylation rate to be 30, 60, and 90 methyls per plasmid.…”

Section: Methodsmentioning

confidence: 99%

TATA Binding Protein Discriminates between Different Lesions on DNA, Resulting in a Transcription Decrease

Coin

Frit

Viollet

et al. 1998

Molecular and Cellular Biology

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DNA damage recognition by basal transcription factors follows different mechanisms. Using transcriptioncompetition, nitrocellulose filter binding, and DNase I footprinting assays, we show that, although the general transcription factor TFIIH is able to target any kind of lesion which can be repaired by the nucleotide excision repair pathway, TATA binding protein (TBP)-TFIID is more selective in damage recognition. Only genotoxic agents which are able to induce kinked DNA structures similar to the one for the TATA box in its TBP complex are recognized. Indeed, DNase I footprinting patterns reveal that TBP protects equally 4 nucleotides upstream and 6 nucleotides downstream from the A-T (at position ؊29 of the noncoding strand) of the adenovirus major late promoter and from the G-G of a cisplatin-induced 1,2-d(GpG) cross-link. Together, our results may partially explain differences in transcription inhibition rates following DNA damage.Many carcinogens and antitumor agents structurally modify DNA, often at specific DNA sequences, with as a consequence the disturbance of mechanisms which govern cell life. Following DNA damage, one observes cell cycle arrests in G 2 /M and G 1 phases and a decrease in the rate of transcription. Investigations aimed at elucidating how cells respond to DNA damage evidenced a transcriptionally connected subpathway of DNA repair, called nucleotide excision repair (NER), in which lesions in transcribed genes were preferentially repaired (4,28). This connection between the two mechanisms was further and definitively established when it was demonstrated that the multiprotein complex TFIIH, essential for protein-encoding gene transcription, was also fundamental for NER (for reviews, see references 16 and 36).One of the first steps of any repair process is recognition of the damage, and thus, significant studies have been devoted to identifying proteins able to bind specifically to cisplatin-or UV-induced lesions (for a review, see reference 5). In an effort to understand how TFIIH shuttles between the transcription template and the DNA lesion, we surprisingly demonstrated that TATA binding protein (TBP)-TFIID, another essential basal transcription factor which normally recognizes the TATA box sequence located 30 bp upstream from the transcription start site, also interacts with damaged DNA (41).Before trying to understand the putative role of TBP in DNA repair, we considered it worthwhile to expand our investigations examining the connection between these two essential transcription components, TFIIH and TFIID, and several damaged DNAs. Seven different drugs ( Fig. 1 and Table 1) which bind covalently to DNA were chosen. The platinum derivatives form mono-or bifunctional adducts with DNA. First, the diethylenetriaminedichloroplatinum(II) derivative (Dien) (24) was chosen for its ability to form a monofunctional adduct recognized by the NER pathway in bacteria (2). Cisplatin (CDDP), transplatin (TDDP), and dachplatin (Dach) were used for their capacity to induce monofunctional adducts which ...

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“…Other DNA lesions, including 8-hydroxyadenine and 2,6-diamino-4-hydroxy-5-formamidepyrimidine (Fapy), can be repaired by Ogg1 (12,13). Ringopened lesions like Fapy are known to inhibit DNA synthesis and may be highly toxic (14,15). Alternatively, the irradiation may cause the formation of 8-hydroxyguanine that may be toxic rather than mutagenic due to the speciˆc locations in which it was formed.…”

Section: Resultsmentioning

confidence: 99%

Oxidative DNA Damage Induced by 364-nm UVA Laser in Yeast Cells

Negishi

Higashi

Nakamura

et al. 2006

Genes and Environment

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The mechanisms of the toxic eŠects of UVA (320-400 nm) irradiation remain unclear. The actions of monochromatic longer wavelength UVA, in particular, have been di‹cult to analyze because of a lack of a powerful light source; however, a UVA laser that can be used for biological studies was recently developed. In the current studies, we examined the eŠects of 364-nm irradiation on yeast cells using a potent UVA laser. We found that, when irradiated under aerobic conditions, yeast cells lacking Ogg1 glycosylase were more sensitive than those with Ogg1. The ability of the 364-nm light to kill the yeast cells was almost eliminated by purging with argon gas. The mutagenic eŠects of the UVA irradiation did not appear to be enhanced by a lack of Ogg1. These results indicate the killing of yeast cells by 364-nm UVA may be dependent on oxidation and may involve DNA lesions that can be repaired by Ogg1.

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Biological properties of imidazole ring-opened N7-methylguanine in M13mp18 phage DNA

Cited by 71 publications

References 43 publications

Effects of a Guanine-derived Formamidopyrimidine Lesion on DNA Replication

Effects of a Guanine-derived Formamidopyrimidine Lesion on DNA Replication

TATA Binding Protein Discriminates between Different Lesions on DNA, Resulting in a Transcription Decrease

Oxidative DNA Damage Induced by 364-nm UVA Laser in Yeast Cells

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