Thiol and hydrogen peroxide modification of recA induction in UV-irradiated wild-type and catalase-deficient Escherichia coli K12.
Induction of recA in Escherichia coli, monitored as beta-D-galactosidase (beta-Gal) activity in recA-lacZ fusion strains, was shown to be elevated and prolonged by dithiothreitol (DTT) treatment after far-UV radiation. Pretreatment of UV-irradiated cultures using DTT led to a shortened recA response and little increase of beta-Gal yield. Similar studies were performed using a catalase-deficient recA-lacZ strain in which the major feature was elevated levels of recA-lacZ induction. Catalase activity in UV-irradiated wild-type cells was reduced by DTT treatment to levels as low as in a katE mutant strain, leading to similar recA-lacZ induction patterns between the strains. Neither DTT nor H2O2 treatment of cells could induce significant recA transcription in the absence of UV-radiation, implying that both agents modify recA activity primarily by interfering with repair of recA-inducing DNA lesions. The results confirm previous studies suggesting that modification of DNA repair is probably a significant portion of thiol radiation protection.
Claycamp
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Radiation Biology Program, University of Iowa, Iowa City 52242.
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DeRose
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D020642:Acatalasia; D003001:Cloning, Molecular; D004229:Dithiothreitol / Q000494:pharmacology*; D004926:Escherichia coli / Q000187:drug effects / Q000201:enzymology / Q000235:genetics* / Q000528:radiation effects; D015964:Gene Expression Regulation, Bacterial / Q000187:drug effects / Q000528:radiation effects; D006861:Hydrogen Peroxide / Q000494:pharmacology*; D009195:Peroxidase / Q000172:deficiency; D011938:Rec A Recombinases / Q000096:biosynthesis / Q000235:genetics*; D014466:Ultraviolet Rays; D001616:beta-Galactosidase / Q000235:genetics
D006861:Hydrogen Peroxide; D009195:Peroxidase; D011938:Rec A Recombinases; D001616:beta-Galactosidase; D004229:Dithiothreitol