Expression of the E. coli uvrA gene is inducible

Abstract

UvrA⁺-dependent excision repair^{1, 2} is one of the most important systems in Escherichia coli for repairing UV-induced pyrimidine dimers¹ and a variety of other forms of DNA damage^{3, 4}. The uvrA protein acts in conjunction with the uvrB and uvrC gene products to introduce a nick at the site of a DNA lesion and thus initiate the repair process¹. We have recently used the Mud(Ap, lac)⁵ operon fusion vector to identify a set of genes whose expression is induced by DNA damage. One Mud(Ap, lac) insertion mapped at the uvrA locus and made the cells sensitive to UV light. In this fusion strain, β-galactosidase expression was induced by DNA-damaging agents in a recA⁺ lexA⁺-dependent fashion⁶. We were surprised by this result because uvrA⁺-dependent excision repair is observed both in cells in which protein synthesis has been inhibited⁷ and in recA⁻ and lexA⁻ cells⁸, findings which have led to the conclusion that the uvrA gene product is constitutively expressed and not under the control of the complex recA⁺lexA⁺ regulatory circuitry⁹ (see below). We have investigated this possibility further and describe here the generation and characterization of a set of fusions of the lac genes to the promoter of the uvrA gene. We confirm that the uvrA gene product is induced by DNA damage in a recA⁺lexA⁺-dependent fashion.