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J Bacteriol. 1991 September; 173(17): 5564-5567

research-article

Novobiocin-dependent topA deletion mutants of Escherichia coli.

G G Hammond, P J Cassidy and K M Overbye

Merck Sharp and Dohme Research Laboratories, Merck and Co., Inc., Rahway, New Jersey 07065-0900.

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.

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J Bacteriol. 1991 September; 173(17): 5564-5567