From DNA damage to mutation in mammalian cells: A review

Rossman, Toby G.; Klein, Catherine B.

doi:10.1002/em.2850110111

Cited by 18 publications

(7 citation statements)

References 119 publications

(36 reference statements)

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“…Inducible responses are also found in eukaryotic cells, but mutagenesis does not appear to conform to the bacterial SOS model [21]. This explains the lack of mutagenicity in mammalian cells.…”

Section: Discussionmentioning

confidence: 98%

Correlation between umuC induction and Salmonella mutagenicity assay for quinolone antimicrobial agents

Power¹

1993

FEMS Microbiology Letters

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Quinolone antimicrobial agents induce the SOS response in bacteria, including the umuDC genes necessary for error-prone repair. Consequently these drugs may be mutagenic in bacteria with a functional SOS response. Differential killing tests with Escherichia coli WP2 (trp) and its repair-deficient derivative CM871 (trp lexA recA uvrA) indicated that a functional DNA repair system was protective against the action of quinolones, implying that quinolones are causing some form of DNA damage (not necessarily directly) and are therefore genotoxic. Dose-dependent reversion from His- to His+ with quinolones was observed in the Ames test with Salmonella typhimurium TA102 (uvr+) but in no other Salmonella tester strains (all uvr-), suggesting that a functional excision repair system is essential for quinolone-induced bacterial mutagenesis. A significant correlation between SOS inducing potential (SOSIP) and mutagenic potential in the Ames test (r = 0.89) indicated that quinolone-induced mutagenic effects in bacteria are almost entirely due to SOS-processed DNA damage.

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Section: Discussionmentioning

confidence: 98%

Correlation between umuC induction and Salmonella mutagenicity assay for quinolone antimicrobial agents

Power¹

1993

FEMS Microbiology Letters

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“…For more detailed treatments of various aspects of the SOS response in bacteria and mammalian cells, other recent reviews are recommended: the SOS response in E. coli [Witkin, 1976;Oishi et al, 1981; Little and Mount, 1982;Gottesman, 1984;Walker, 19841; pKMlOl [Strike and Lodwick, 19871; lambda prophage induction [Roberts and Devoret, 1983;Elespuru, 19841; DNA repair [Hanawalt et al, 1979;Defais et al, 1983;Walker et al, 19851; the SOS response in mammalian cells [Radman, 1980;Sarasin, 1985; Rossman and Klein, 1985; Lambert and Garrels, 19861.…”

Section: Introductionmentioning

confidence: 99%

“…The mechanistic basis in E. coli for one of the SOS responses, mutagenesis, is currently a subject of intensive study in many laboratories, and recent developments in this area are explored in greater detail. Mutagenesis in mammalian cells, which does not appear to conform to the SOS model, is the subject of a forthcoming review [Rossman and Klein, in press].For more detailed treatments of various aspects of the SOS response in bacteria and mammalian cells, other recent reviews are recommended: the SOS response in E. coli [Witkin, 1976;Oishi et al, 1981;Little and Mount, 1982; Gottesman, 1984; Walker, 19841; pKMlOl [Strike and Lodwick, 19871; lambda prophage induction [Roberts and Devoret, 1983; Elespuru, 19841; DNA repair [Hanawalt et al, 1979;Defais et al, 1983; Walker et al, 19851; the SOS response in mammalian cells [Radman, 1980;Sarasin, 1985;Rossman and Klein, 1985; Lambert and Garrels, 19861. The contents of this publication do not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the US Government.…”

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confidence: 99%

“…The search for mammalian equivalents of DNA damage-inducible functions was hindered by the lack of analogous mutants in mammalian cells. Early experiments sought evidence for the phenomenology of the bacterial SOS system in mammalian cells (reviewed in Hewitt and Meyn [ 19781, Radman [ 19801, Stone-Wolff and Rossman [1981], Witkin [ 19841, Sarasin [1985], and Rossman and Klein [1985]). This included reactivation and mutagenesis of viruses, error-prone repair, induction of resident viruses, and the induction of proteases.…”

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confidence: 99%

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Inducible responses to dna damage in bacteria and mammalian cells

Elespuru¹

1987

Environ and Mol Mutagen

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INTRODUCTIONThis review summarizes current knowledge of the DNA damage-inducible SOS response in E. coli, with an emphasis on the historical development of experimentation in this area. Evidence for the existence of analogous responses to DNA damage in other bacteria, lower eukaryotes, and mammalian cells is also presented. The mechanistic basis in E. coli for one of the SOS responses, mutagenesis, is currently a subject of intensive study in many laboratories, and recent developments in this area are explored in greater detail. Mutagenesis in mammalian cells, which does not appear to conform to the SOS model, is the subject of a forthcoming review [Rossman and Klein, in press].For more detailed treatments of various aspects of the SOS response in bacteria and mammalian cells, other recent reviews are recommended: the SOS response in E. coli [Witkin, 1976;Oishi et al, 1981;Little and Mount, 1982; Gottesman, 1984; Walker, 19841; pKMlOl [Strike and Lodwick, 19871; lambda prophage induction [Roberts and Devoret, 1983; Elespuru, 19841; DNA repair [Hanawalt et al, 1979;Defais et al, 1983; Walker et al, 19851; the SOS response in mammalian cells [Radman, 1980;Sarasin, 1985;Rossman and Klein, 1985; Lambert and Garrels, 19861. The contents of this publication do not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the US Government.By acceptance of this article, the publisher or recipient acknowledges the right of the US Government to retain a nonexclusive, royalty-free license in and to any copyright covering the article.Published 1987 by Alan R. Liss, Inc. Elespuru THE SOS RESPONSE IN E. coliObservations of apparently unrelated phenomena (virus reactivation, mutagenesis, prophage induction, filamentation) in different genetic backgrounds in E. coli led to a unifying hypothesis called the "SOS response" [Radman, 19751. The "SOS" hypothesis suggested "the existence of a DNA repair system which is normally repressed but which is induced by DNA damage". Two early concepts were critical to the development of the SOS model. One was that mutagenesis and repair of DNA damage depended on an inducible cellular process [Sedgewick, 1975; Witkin, 19761. This concept developed from the experiments of Weigle and others, which showed that survival and mutagenesis of UV-irradiated lambda phage depended on the irradiation of the host E. coli and was inhibited by the presence of chloramphenicol Weigle, 1953; Defais et al, 19761. The second concept, of coordinate regulation of responses to DNA damage, arose from genetic experiments. Mutations in certain genes (rec and lex) resulted in the abolition of all of the known responses to genetic damage under study (Weigle reactivation, mutagenesis, lambda prophage induction, filamentation) or to their temperature-dependent expression witkin, 1967, 1969; Castellazzi et al, 1972; Ishii and Kondo, 19751. The abolition of "Weigle reactivation" (enhanced survival o...

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“…It is clear that an important component of the mutagenic process is misreplication of damaged DNA (4,24). The role of indirect effects of DNA-damaging agents in the mutagenic process in mammalian cells is less well understood.…”

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confidence: 99%

Use of a simian virus 40-based shuttle vector to analyze enhanced mutagenesis in mitomycin C-treated monkey cells.

et al. 1988

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When monkey cells were treated with mitomycin C 24 h before transfection with UV-irradiated pZ189 (a simian virus 40-based shuttle vector), there was a twofold increase in the frequency of mutations in the supF gene of the vector. These results suggest the existence of an enhancible mutagenesis pathway in mammalian cells. However, DNA sequence analysis of the SupF-mutants suggested no dramatic changes in the mechanisms of mutagenesis due to mitomycin C treatment of the cells.Exposure of mammalian cells to a wide variety of DNAdamaging agents can lead to mutagenesis and cellular transformation. It is clear that an important component of the mutagenic process is misreplication of damaged DNA (4, 24). The role of indirect effects of DNA-damaging agents in the mutagenic process in mammalian cells is less well understood. In bacterial systems, indirect effects of DNAdamaging agents play a major role in mutagenesis; induction of the bacterial SOS system is required for damage-directed mutagenesis to occur (3,10,31). Evidence for analogous indirect effects in mammalian systems comes primarily from studies on enhanced viral reactivation and mutagenesis (reviewed in references 3, 24, and 25). When mammalian cells are pretreated with a DNA-damaging agent before infection with a UV-irradiated virus, virus survival is enhanced over that observed in untreated cells. Although this enhancement of survival is often accompanied by enhancement of mutagenesis, this correlation has not been observed in all systems (2,20,25,26,30). Nothing is known about the molecular mechanisms involved in enhanced mutagenesis in mammalian cells.To gain a better understanding of enhanced mutagenesis in mammalian cells, we used the simian virus 40-based shuttle vector pZ189 (28). This vector replicates in both primate and bacterial cells and contains the bacterial supF suppressor gene as an easily sequenced mutagenesis target. We analyzed the frequency and sequence characteristics of mutants induced when either UV-damaged or undamaged pZ189 templates replicate in monkey cells pretreated with the DNA-damaging agent mitomycin C. Since the vector DNA and the mammalian cells can be treated independently with DNA-damaging agents, we could assess both direct and indirect effects of the agents on the mutagenic process. UV radiation was chosen as the DNA-damaging agent for the vector DNA because the mutagenic action of this agent has been extensively studied in the pZ189 system (1,6,18 with antibiotics and 5% fetal bovine serum were treated with mitomycin C (1 ug/Iml) in serum-free Dulbecco minimal essential medium for 2.5 h. The mitomycin C-containing medium was then removed, the cells were washed, and fresh medium with 2% serum was added to the dishes. At 24 h later, the medium was removed and saved, the cells were transfected with 100 ng of pZ189 plasmid DNA (either UV irradiated [6] or not irradiated) per 100-mm dish by the DEAE-dextran method (11), and then the conditioned medium was added. At 48-h later, plasmid DNA was extracted from the cells by the...

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From DNA damage to mutation in mammalian cells: A review

Cited by 18 publications

References 119 publications

Correlation between umuC induction and Salmonella mutagenicity assay for quinolone antimicrobial agents

Correlation between umuC induction and Salmonella mutagenicity assay for quinolone antimicrobial agents

Inducible responses to dna damage in bacteria and mammalian cells

Use of a simian virus 40-based shuttle vector to analyze enhanced mutagenesis in mitomycin C-treated monkey cells.

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