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.