Ultraviolet mutagenesis and inducible DNA repair in Escherichia coli.

Witkin, Evelyn M.

doi:10.1128/mmbr.40.4.869-907.1976

Cited by 1,171 publications

(380 citation statements)

References 150 publications

(224 reference statements)

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“…The influence of UVC with a wavelength of 254 nm on bacterial DNA results mainly in the formation of thymine dimers, which stop the correct reading of genetic information and, thus, lead to the death of a bacterial population [Witkin, 1976;Sancar and Sancar, 19881. Certain enzymatic repair pathways in the cells are responsible for eliminating the damaged sites of DNA; these pathways include a light-dependent photoreactivation system, a dark repair system, and a lightindependent SOS repair system [Witkin, 1976;Little and Mount, 1982;Seeberg and Steinum, 1983;Lin and Sancar, 1992;West and Connolly, 19921. Certain genes in E. coli chromosomes encode the synthesis of enzymes that play key roles on different stages of the DNA dark repair system.…”

Section: Discussionmentioning

confidence: 99%

“…Certain genes in E. coli chromosomes encode the synthesis of enzymes that play key roles on different stages of the DNA dark repair system. These roles include: 1) detection of the dimers, primary incision, and, then, excision of the damaged fragment (genes uvrA, uvrB, and uvrC) [Seeberg and Steinum, 1983;Lin and Sancar, 1992;West and Connolly, 19921; 2) synthesis of the complementary strand of DNA (polA); and 3) sealing the gap between a newly formed fragment and the rest of DNA (ligA) [Witkin, 1976;Sancar and Sancar, 19881. Because our experiments were performed in a dark environment, it is most likely that the dark repair system is activated directly or indirectly by mm waves.…”

Section: Discussionmentioning

confidence: 99%

“…Golant et al [1983] and Bryukhova et al [1985] have suggested the possibility of increasing the effect of mm waves by exposure of the organisms to the destabilizing action of some other physical or chemical agent just before or after the microwave irradiation. In the present study, we chose UVC light as an additional damaging factor, because it can be easily applied and measured, and the mechanisms responsible for the lethal effects of UV light on cell structures, primarily DNA, have been studied extensively [Witkin, 1976;Sancar and Sancar, 1988;Lin and Sancar, 1992;Levy et al, 19933. Our results are reported and discussed below.…”

Section: Influence Of MM Waves Only On E Colimentioning

confidence: 99%

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Effect of millimeter waves on survival of UVC‐exposed Escherichia coli

Rojavin

Ziskin

1995

Bioelectromagnetics

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Bacterial cells of the strain Escherichia coli K12 were exposed to millimeter electromagnetic waves (mm waves) with and without additional exposure to ultraviolet light lambda = 254 nm (UVC). The mm waves were produced by a medical microwave generator emitting a 4-GHz-wide band around a 61 GHz center frequency and delivering an irradiation of 1 mW/cm2 and a standard absorption rate (SAR) of 84 W/kg to the bacteria. Exposure to the mm waves alone for up to 39 minutes did not change the survival rate of bacteria. Exposure to mm waves followed by UVC irradiation also did not alter the number of surviving E. coli cells in comparison to UVC-treated controls. When mm waves were applied after the UVC exposure, a dose-dependent increase of up to 30% in the survival of E. coli was observed compared to UVC + sham-irradiated bacteria. Because sham controls and experimental samples were maintained under the same thermal conditions, the effect is not likely to be due to heating, although the possibility of nonuniform distribution of microwave heating in different layers of irradiated bacterial suspension cannot be ruled out. The mechanism for this effect appears to involve certain DNA repair systems that act as cellular targets for mm waves.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Influence Of MM Waves Only On E Colimentioning

confidence: 99%

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Effect of millimeter waves on survival of UVC‐exposed Escherichia coli

Rojavin

Ziskin

1995

Bioelectromagnetics

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“…4, 5, and 7) is due primarily, if not exclusively, to amebae and not to residual bacteria, a small number of which inevitably persist after washing [ 151 . In the case of methionine, cycloheximide, an inhibitor that does not inhibit prokaryotic protein synthesis [31] , completely inhibits incorporation, as shown in Figure 4. The limited number of proteins synthesized, particularly in control cells (Fig.…”

Section: Scussl Onmentioning

confidence: 93%

Induction of multiple flagella in Naegleria: Requirements for RNA and protein synthesis

1979

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The induction of multiple flagella by a heat shock was used to examine the role of RNA and protein synthesis in the regulation of the number of flagella produced during the differentiation of the amebo-flagellate Naegleria gruheri. Control cells differentiating at 25.0"C produce an average of 2.1 flagella per flagellate (f/F), whereas cells exposed t o 38.2'C from 35 minutes until 72 minutes after initiation produce an average of approximately 5 f/F. Heat shock was found t o prevent completion of the RNA synthesis essential for flagelluF formation, even though both RNA and protein synthesis continued a t 38.2 C . A delay of two minutes for every one minute of heat shock was seen in both the formation of flagella (TSo) and the completion of essential RNA synthesis for heat shocks of one to ten minutes applied beginning 35 minutes after initiation. Times at 38.2"C of ten minutes t o 45 minutes produced a delay of approximately 0.6 minutes for each minute of heat shock, whereas shocks longer than 47 minutes prevented flagellum formation. The times from completion of RNA synthesis until completion of protein synthesis or flagella formation were found to be approximately 15 minutes and approximately 32 minutes, respectively. This was true in control cells as well as in cells heat shocked for up t o 45 minutes. The fact that heat shock delayed completion of RNA synthesis without affecting the time for completion of protein synthesis or flagella formation suggests that heat shock acts at some step related t o the completion of transcription. Short heat shocks, 3 0 seconds t o five minutes, were observed to prevent flagellum formation in cells that had completed RNA synthesis if additional RNA synthesis was inhibited. In contrast, short heat shocks had little effect on cells that had completed protein synthesis, even if additional protein synthesis was inhibited. Two alternative hypotheses for the mechanism of heat shock delay of transcription are discussed. One hypothesis involves a direct effect of high temperature on transcription, and the other postulates a temperature-sensitive protein necessary for flagellum formation.

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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%

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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Ultraviolet mutagenesis and inducible DNA repair in Escherichia coli.

Cited by 1,171 publications

References 150 publications

Effect of millimeter waves on survival of UVC‐exposed Escherichia coli

Effect of millimeter waves on survival of UVC‐exposed Escherichia coli

Induction of multiple flagella in Naegleria: Requirements for RNA and protein synthesis

Inducible responses to dna damage in bacteria and mammalian cells

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