title: Novobiocin-dependent topA deletion mutants of Escherichia coli.
abstract: Previous reports of the transduction of topA deletions in Escherichia coli suggested that delta top A transductants grow normally only if they acquire spontaneous mutations that compensate for the topoisomerase I defect. We show that P1-mediated transduction of delta topA in the presence of sublethal concentrations of novobiocin, an inhibitor of the DNA gyrase B subunit, yields uncompensated Top- isolates which are dependent on novobiocin for optimum growth. In the absence of novobiocin these delta topA strains grow slowly, indicating that topA deletions are deleterious but not lethal to the cell. We propose that inhibitors of DNA gyrase B, presumably by lowering intracellular levels of DNA supercoiling, can phenotypically suppress a topoisomerase I defect in E. coli.
authors.affiliation: Merck Sharp and Dohme Research Laboratories, Merck and Co., Inc., Rahway, New Jersey 07065-0900.
authors.forename: G G
authors.initials: GG
authors.lastname: Hammond
authors.forename: P J
authors.initials: PJ
authors.lastname: Cassidy
authors.forename: K M
authors.initials: KM
authors.lastname: Overbye
mesh_terms: D002872:Chromosome Deletion; D004264:DNA Topoisomerases, Type I / Q000235:genetics* / Q000378:metabolism; D004352:Drug Resistance, Microbial / Q000235:genetics; D004926:Escherichia coli / Q000235:genetics / Q000254:growth & development / Q000378:metabolism*; D005798:Genes, Bacterial; D009154:Mutation; D009675:Novobiocin / Q000378:metabolism*; D014161:Transduction, Genetic
chemical_list: D009675:Novobiocin; D004264:DNA Topoisomerases, Type I