Phenotypic difference between uvr A and uvr B mutants of E. coli.

Abstract

THE synthesis of colicin E1, an antibiotic protein, by cells of Escherichia coli is coded for by a bacterial plasmid, colicinogenic factor E1 (ColE1). The synthesis is induced by agents such as ultraviolet light1 or mitomycin C (mit C)2. Ultraviolet and mit C are known to modify the base portions of DNA to form pyrimidine dimers3 and cross linkages between complementary strands4, respectively. Damage to DNA caused by ultraviolet or mit C is repairable by a similar molecular mechanism5,6, but the relationship between these repair systems and the induction process of ColE1 synthesis has not been established unequivocally. We have analysed the induction of the colicin by ultraviolet and mit C in various ultraviolet-sensitive mutants to which the colicinogenic factor was transferred. Among the mutants tested, the recA mutant did not synthesise the colicin in response to ultraviolet or mit C as reported previously7. In addition, however, we have now found that the induction of the colicin synthesis is greatly delayed in the uvrB mutant, but is normal in the uvrA mutant.