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Author (up) Aertsen, A.; Michiels, C.W. file  url
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  Title SulA-dependent hypersensitivity to high pressure and hyperfilamentation after high-pressure treatment of Escherichia coli lon mutants Type Journal Article
  Year 2005 Publication Research in Microbiology Abbreviated Journal Res Microbiol  
  Volume 156 Issue 2 Pages 233-237  
  Keywords Colony Count, Microbial; Culture Media; Escherichia coli--genetics, growth & development; Escherichia coli Proteins--genetics, metabolism; Gene Expression Regulation, Bacterial; Hydrostatic Pressure; Mutation; Protease La--genetics; SOS Response (Genetics); Ultraviolet Rays  
  Abstract High-pressure treatment (>100 MPa) is known to induce several heat shock proteins as well as an SOS response in Escherichia coli. In the current work, we have investigated properties with respect to high-pressure treatment of mutants-deficient in Lon, a pressure-induced ATP-dependent protease that belongs to the heat shock regulon but that also has a link to the SOS regulon. We report that lon mutants show increased pressure sensitivity and exhibit hyperfilamentation during growth after high-pressure treatment. Both phenotypes could be entirely attributed to the action of the SOS protein SulA, a potent inhibitor of the cell division ring protein FtsZ and a specific target of the Lon protease, since they were suppressed by knock-out of SulA. Introduction of the lexA1 allele, which effectively blocks the entire SOS response, also suppressed the high pressure hypersensitivity of lon mutants, but not their UV hypersensitivity. These results indicate the existence of a SulA-dependent pathway of high-pressure-induced cell filamentation, and suggest involvement of the SOS response, and particularly of SulA, in high-pressure-mediated cell death in E. coli strains which are compromised in Lon function.  
  Call Number Serial 301  
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Author (up) Arimoto-Kobayashi, S.; Sakata, H.; Mitsu, K.; Tanoue, H. file  url
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  Title A possible photosensitizer: Tobacco-specific nitrosamine, 4-(N-methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), induced mutations, DNA strand breaks and oxidative and methylative damage with UVA Type Journal Article
  Year 2007 Publication Mutation Research Abbreviated Journal Mutat Res  
  Volume 632 Issue 1-2 Pages 111-120  
  Keywords Base Sequence; DNA Breaks; DNA Methylation--drug effects, radiation effects; Dose-Response Relationship, Drug; Models, Biological; Molecular Sequence Data; Mutation; Nitrosamines--toxicity; Oxidative Stress--drug effects, radiation effects; Photosensitizing Agents--toxicity; Salmonella typhimurium; Tobacco--chemistry; Ultraviolet Rays--adverse effects  
  Abstract We discovered the directly acting mutagenicity of the tobacco-specific nitrosamine, 4-(N-methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), with UVA light (320-400nm) in Ames bacteria and phage M13mp2 in the absence of metabolic activation. We have investigated the spectrum of mutations caused by UVA-activated NNK. The majority (57%) of induced sequence changes were comprised of GC to CG, GC to TA and GC to AT. This suggested that modification of guanine residues was responsible for these mutations. Hence, we explored the formation of 7,8-dihydro-8-oxo-2'-deoxyguanosine (8-oxodG) and O(6)-methylguanine (O(6)meG) in the DNA. When calf thymus DNA was treated with NNK and UVA, the amount of 8-oxodG/dG and O(6)meG/G in the DNA increased up to 20-fold and 100-fold, respectively, compared with the untreated control. DNA strand breaks were observed following NNK and UVA treatment, and the strand breaks were suppressed in the presence of scavengers for oxygen and NO radical. The formation of NO was also observed in NNK solutions irradiated with UVA. We analyzed the photodynamic spectrum of mutation induction, 8-oxodG formation and NO formation using monochromatic radiation. The patterns of the action spectra were comparable to the absorption spectrum of NNK. We conclude that NNK may act as a photosensitizer in response to UVA to produce NO and other oxidative and alkylative intermediates following the formation of 8-oxodG and O(6)meG in DNA, which may lead to mutations and DNA strand breaks.  
  Call Number Serial 86  
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Author (up) Bayliss, C.E.; Waites, W.M. file  url
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  Title Resistance of Serratia marcescens to hydrogen peroxide Type Journal Article
  Year 1981 Publication The Journal of Applied Bacteriology Abbreviated Journal J Appl Bacteriol  
  Volume 50 Issue 1 Pages 131-137  
  Keywords Catalase/metabolism; Drug Resistance, Microbial; Hot Temperature; Hydrogen Peroxide/*pharmacology; Serratia marcescens/*drug effects/enzymology/radiation effects; Ultraviolet Rays  
  Abstract Irradiation with ultraviolet (u.v.) light (71 J/m2) reduced the viable count of suspenrsions of Serratia marcescens, grown in a glycerol-salts defined medium, to five in 104 cells. Subsequent incubation of irradiated cells in hydrogen peroxide failed to decrease the survivors, but u.v. irradiation in the presence of hydrogen peroxide reduced the viable count to fewer than two in 106 cells. Cells grown in defined medium with added iron had more measurable catalase activity and were more resistant to hydrogen peroxide alone and to simultaneous treatment with u.v. irradiation and hydrogen peroxide. Cells grown in a non-defined medium contained little iron and measurable catalase activity but were more resistant to hydrogen peroxide. Treatment with toluene, heat killing or sonication increased the catalase activity detected in all cell suspensions and showed that resistance to hydrogen peroxide and to u.v. irradiation in hydrogen peroxide was related to the total catalase activity within cells.  
  Call Number Serial 489  
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Author (up) Berenstein, D. file  url
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  Title UV-inducible DNA repair in Acinetobacter calcoaceticus Type Journal Article
  Year 1987 Publication Mutation Research Abbreviated Journal Mutat Res  
  Volume 183 Issue 3 Pages 219-224  
  Keywords Acinetobacter/genetics/*radiation effects; Bacteriophages/genetics; Cell Division/radiation effects; DNA Repair/*radiation effects; Lysogeny/radiation effects; Mutation/radiation effects; Ultraviolet Rays  
  Abstract Bacterial mutation frequency after UV irradiation and phage mutation frequency under conditions of W-reactivation were determined in A. calcoaceticus. With the exception of streptomycin resistance, there was no increase in the frequency of the assayed markers above the background level. The increased survival of phage during W-reactivation was not followed by an increase in the frequency of mutation from turbid to clear plaque formers among phage survivors. The findings suggested that the UV-inducible repair pathway in A. calcoaceticus was error free. Post-irradiation incubation of UV-treated culture before phage infection resulted in a further increase of W-reactivation. As chloramphenicol inhibited this response, it was concluded that de novo protein synthesis was involved in the UV-inducible repair pathway in A. calcoaceticus.  
  Call Number Serial 409  
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Author (up) Berenstein, D. file  url
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  Title Weigle reactivation in Acinetobacter calcoaceticus Type Journal Article
  Year 1982 Publication Photochemistry and Photobiology Abbreviated Journal Photochem Photobiol  
  Volume 35 Issue 4 Pages 579-581  
  Keywords Acinetobacter/growth & development/*radiation effects; Bacteriophages/growth & development/*radiation effects; Ultraviolet Rays; Viral Plaque Assay  
  Abstract Weigle (W)-reactivation was demonstrated in Acinetobacter calcoaceticus for the UV-irra-diated lysogenic phage P78. The reactivation factor (survival of irradiated phage on irradiated bacteria/ survival on unirradiated bacteria) reached a maximum value of 20. This was obtained at UV-doses giving phage and host survivals of about 5 times 10-6 and 1 times 10-1, respectively. Intracellular development of W-reactivated P78 was followed by one-step growth experiments. Conditions which allowed maximal W-reactivation also extended the period of phage production and yielded a somewhat reduced burst size.  
  Call Number Serial 412  
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