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Gene Review

topA  -  DNA topoisomerase I

Salmonella enterica subsp. enterica serovar Typhimurium str. LT2

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Disease relevance of topA

  • The leu-500 promoter is inactivated by a mutation in the -10 region but can be activated in topA Escherichia coli and Salmonella strains [1].
  • The leu-500 promoter of Salmonella typhimurium is a mutant and inactive variant of the leucine operon promoter that regains activity if negative DNA supercoiling rises above normal levels, typically as a result of mutations affecting DNA topoisomerase I (topA mutants) [2].

High impact information on topA

  • Furthermore, when cloned onto a multicopy plasmid, the leu-500 promoter failed to function, even in a topA background [3].
  • Activation of the leu-500 promoter was analysed in topA mutant cells harbouring transcriptionally inducible tet or cat gene cassettes inserted in the region upstream from the leu operon [2].
  • Mutations affecting DNA topoisomerase I (topA) in Salmonella typhimurium were isolated and graded on the basis of their ability to reverse the effects of gyrB mutations on his operon expression [4].
  • Nevertheless, invA was poorly expressed in topA mutants of S. typhimurium, which have increased DNA superhelicity [5].
  • This position-dependent supercoiling effect on gene activation is best illustrated in the study of the suppression of the leu-500 mutation of the leuABCD operon in a Salmonella typhimurium topA mutant [6].

Biological context of topA

  • Expression of the lacZ gene from the supercoiling-sensitive leu-500 promoter on a plasmid in topA mutant cells was stimulated by activating a divergently oriented Tac promoter, 400 bp upstream from leu-500 [7].
  • Using the suppression of the leu-500 mutation in Salmonella typhimurium topA mutants as a model system, we put forward our view of the effects of transcription-driven DNA supercoiling on gene expression control [8].

Associations of topA with chemical compounds

  • S. typhimurium strains carrying either point or deletion mutations in topA had previously been shown to lose their mutability by UV or methyl methanesulfonate (K. Overbye and P. Margolin, J. Bacteriol. 146:170-178, 1981; K. Overbye, S. M. Basu, and P. Margolin, Cold Spring Harbor Symp. Quant. Biol. 47:785-791, 1983) [9].


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