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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Archives of microbiology 129 (1981), S. 67-71 
    ISSN: 1432-072X
    Keywords: Bioluminescence ; Marine bacteria ; Electron transport ; Low oxygen ; Long-chain aldehyde ; Luciferase expression quotient
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The in vivo expression of cellular bacterial luciferase has been defined as the luciferase expression quotient, measured as the ratio of the bioluminescence intensity in vivo to the in vitro activity of luciferase in crude cell extracts. The expression is greater in the presence of inhibitors of the electron transport system such as cyanide and N-heptyl-4-hydroxyquinoline and also at lower oxygen tensions. The higher expression of the cellular luciferase under these conditions is postulated to be due to an increase in the intracellular levels of reduced coenzymes which enhance both the reduction of flavin and the reduction of fatty acid to aldehyde. Both FMNH2 and aldehyde are substrates in the light emitting reaction.
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  • 2
    Electronic Resource
    Electronic Resource
    New York : Wiley-Blackwell
    Journal of Bioluminescence and Chemiluminescence 2 (1988), S. 95-99 
    ISSN: 0884-3996
    Keywords: Bioluminescence ; genotoxicity ; Photobacterium fischeri ; Chemistry ; Biochemistry and Biotechnology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Twenty metallic compounds were assayed for their genotoxic mutagenic activity by the bioluminescence test restoration of the luminescence of dark mutant of the luminous bacterium Photobacterium fischeri). The activity of the metals was tested in a liquid medium as well as on a solid medium. K2Cr2O7, MnCl2, BeCl2, KH2AsO4, ZnCl2 and Na2WO4 showed strong activity in liquid medium while AgNO3, Cd(OOCCH3)2, CoCl2, CuCl2, HgCl2, Na2SeO3 and Pb(NO3)2 were more active in the solid medium test. BaCl2, Na2MoO4, NaAsO2, NiSO4, Na2SeO4, RbCl, and SnCl2 were not active in the bioluminescence test. The correlation between the genotoxic activity of the tested metallic compounds in the bioluminescence test and other bacterial tests for genotoxic agents as well as the correlation between these results and the carcinogenicity of these compounds is discussed.
    Additional Material: 2 Ill.
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  • 3
    Electronic Resource
    Electronic Resource
    New York : Wiley-Blackwell
    Journal of Bioluminescence and Chemiluminescence 2 (1988), S. 81-93 
    ISSN: 0884-3996
    Keywords: Bioluminescence ; Sigma 32 ; luciferase ; Chemistry ; Biochemistry and Biotechnology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Luminescence in the marine bacterium, Vibrio fischeri, is regulated by a small molecule, the autoinducer. The transcription of the V. fischeri lux genes also requires a regulatory protein, (luxR), cAMP and CRP. We show that, apart from these components, the transcription of the PR lux operon is also controlled by the activity of σ32 (htpR protein). In luminescent Escherichia coli (E. coli/pChv1), as well as in different marine luminous bacteria and their naturally occurring dark (K) variants, the luminescence system can be induced by starvation under microaerophilic conditions. Heat shock also induces luminescence in htpR+ but not in htpR- strains of E. coli/pChv1.An htpR- mutant of E. coli containing pChv1 is very dim and its luminescence is not induced by starvation or heat shock. The addition of a plasmid bearing the gene for htpR+ into such cells restores their response to starvation and heat shock. Cells of wild type E. coli/pChv1 that have been starved or heat shocked respond to lower concentrations of V. fischeri inducer than untreated cells. These cultures also produce more extracellular inducer than untreated cells. Starvation, heat shock and the presence of σ32 do not induce luminescence in luxl deleted E. coli/pChv1 cells.SOS-inducing agents advance the onset of luminescence in both htpR+ and htpR- strains but not in luxl deleted E. coli/pChvi cells.DNA sequencing of the luxR-luxl region reveals the presence of a promoter region of the kind typical for σ32 at the beginning of the luxl gene. In addition we find a LexA protein-DNA binding site in the non-consensus sequence for the -35 region of the PR operon. It is proposed that the regulatory protein-inducer complex displaces the LexA protein and allows the transcription of the right operon. SOS-inducing agents result in proteolysis of LexA protein and advance the onset of luminescence. σ32 enhances the transcription from the PR operon and thus initiates a positive control circuit. It seems that σ32 is the major controlling element in determining the onset of luminescence both in vivo and in vitro.
    Additional Material: 14 Ill.
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