Hypochlorous acid activates the heat shock and soxRS systems of Escherichia coli

Appl Environ Microbiol. 1996 Nov;62(11):4003-8. doi: 10.1128/AEM.62.11.4003-4008.1996.


A series of plasmids, containing fusions of different stress promoters to lux reporter genes, was used in an attempt to monitor the defense circuits activated upon exposure of Escherichia coli to sublethal doses of free chlorine. A significant level of activation was exhibited by promoters of three heat shock genes (grpE, dnaK, and lon), in an rpoH-dependent manner. The promoter of micF, a gene under the control of the soxRS regulon, was also strongly induced, but not in a soxR mutant. This induction was not affected by sodA and sodB mutations, implying that it did not involve oxygen radical activity. Free-chlorine activation of both heat shock and soxRS regulons required an exposure of less then I s in duration. The oxyR or the SOS regulons were apparently not induced by free chlorine (as judged by lack of activation of katG and recA, respectively), and neither was the universal stress (uspA) protein.

MeSH terms

  • Bacterial Proteins / genetics*
  • Escherichia coli / drug effects*
  • Escherichia coli / genetics*
  • Escherichia coli / metabolism
  • Escherichia coli Proteins*
  • Gene Expression Regulation, Bacterial / drug effects
  • Genes, Bacterial / drug effects
  • Heat-Shock Proteins / genetics*
  • Hypochlorous Acid / pharmacology*
  • Mutation
  • Promoter Regions, Genetic
  • Regulon
  • Sigma Factor / genetics
  • Superoxides / metabolism
  • Trans-Activators*
  • Transcription Factors / genetics*


  • Bacterial Proteins
  • Escherichia coli Proteins
  • Heat-Shock Proteins
  • Sigma Factor
  • Trans-Activators
  • Transcription Factors
  • heat-shock sigma factor 32
  • Superoxides
  • SoxR protein, Bacteria
  • SoxS protein, E coli
  • Hypochlorous Acid