A model on the induction by UV irradiation of Escherichia coli bacteria lysogenic with the bacteriophage Lambda

Abstract

The induction of Lambda prophages in lysogenic Escherichia coli cells is started after inactivation of repressor molecules coded for by the prophage genome itself. All agents known to inhibit bacterial DNA synthesis are able to initiate a set of processes resulting in the inactivation of these repressors. I n the case of UV light as an inducing agent i t is suggested that the UV mediated damages within the bacterial DNA diminish the replication velocity leading through a set of intermediate processes t o the inactivation of phage repressors by accumulation of repressor inactivating precursors of DNA synthesis. The analytical function for the dose effect curve is obtained from the product of the probability PI of cells containing I UV damages multiplied by the number 1 of UV damages after summing up all possible numbers of E. The probability of P i is calculated on the basis of the radiation kinetic model of R O N T~ et al. (1972). The theoretical dose effect curve, obtained shows a shoulder with an extrapolation number of 1.2 and a linear part a t high irradiation doses in semilogarithmic plot. The experimental data obtained with UV induction of E . coli K12 (A) are consistent with the model and show that only a few UV damages smaller than 10 per bacterial chromosome are sufficient for induction.The lysogenic complex E . coli-phage Lambda contains the genome of the bacteriophage linearely integrated within the bacterial chromosome as a socalled prophage. The genetic information of this prophage is repressed by the action of repressor molecules coded for by the CI gene of the prophage. This CI gene is the only one which is not under negative control of repressors. All agents known to inhibit DNA synthesis such as mitomycine C treatment or thymine starvation or UV irradiation lead to the induction of vegetative phage development by lifting the repression capacity of the phage repressors. Thereafter, the prophage is excised and autonomously replicated. The biological detectable effect is the lysis of cells or the formation of infective phage particles or the loss of colony forming ability (for review see HERSHEY 1971). By several authors (GOLDTHWAIT and JACOB 1964, RUFX et al. 1971 it has been shown that after the stop of DNA synthesis some DNA precursors are accumulated resulting directly or indirectly in the inactivation of phage repressor molecules. In the case of UV irradiation used as inducing agent it should be proved whether the radiation kinetic model presented by R O N T~ et al. (1967) and developed to the special problem of UV mediated inactivation of phage repressors, is consistent with experimental data obtained from E. coli lysogenic with phage Lambda.