Further characterization of repair of 8-methoxypsoralen crosslinks in UV-excision-defective Escherichia coli.

Evidence was previously presented for a new pathway for the repair of 8-methoxypsoralen DNA crosslinks. The pathway, which is independent of the uvrA gene but deficient in rep mutants, has now been further characterized and shown to be more active in minimal than in nutrient growth media and to be inhibited by acriflavine. Although crosslink repair is much reduced in recA bacteria, some still occurs as judged by the effect of acriflavine. By the same criterion, crosslink repair occurs in bacteria with point mutations in the uvrA and uvrB genes, in bacteria with a deletion covering the uvrB gene, and in polA uvrA bacteria. Bacteria with insertions rather than point mutations in the uvrA gene, although showing evidence of repair, demonstrated minimal inhibition with acriflavine suggesting the possibility that the uvrA gene product, even if enzymically inactive, might be able to interact with DNA lesions in the presence of acriflavine and prevent crosslink repair. Crosslink repair in E. coli WP2 uvrA is associated with base-pair substitution mutagenesis and may be characterized as an error-prone process. Crosslink repair in uvrA bacteria is reduced but not eliminated by a mutation in the umuC gene.