The SOS response is permitted in Escherichia coli strains deficient in the expression of the mazEF pathway

PLoS One. 2014 Dec 3;9(12):e114380. doi: 10.1371/journal.pone.0114380. eCollection 2014.


The Escherichia coli (E. coli) SOS response is the largest, most complex, and best characterized bacterial network induced by DNA damage. It is controlled by a complex network involving the RecA and LexA proteins. We have previously shown that the SOS response to DNA damage is inhibited by various elements involved in the expression of the E. coli toxin-antitoxin mazEF pathway. Since the mazEF module is present on the chromosomes of most E. coli strains, here we asked: Why is the SOS response found in so many E. coli strains? Is the mazEF module present but inactive in those strains? We examined three E. coli strains used for studies of the SOS response, strains AB1932, BW25113, and MG1655. We found that each of these strains is either missing or inhibiting one of several elements involved in the expression of the mazEF-mediated death pathway. Thus, the SOS response only takes place in E. coli cells in which one or more elements of the E. coli toxin-antitoxin module mazEF or its downstream pathway is not functioning.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptation, Physiological
  • Bacteriophage lambda / physiology
  • DNA-Binding Proteins / genetics*
  • DNA-Binding Proteins / metabolism
  • Endoribonucleases / genetics*
  • Endoribonucleases / metabolism
  • Escherichia coli / genetics*
  • Escherichia coli / metabolism
  • Escherichia coli / virology
  • Escherichia coli Proteins / genetics*
  • Escherichia coli Proteins / metabolism
  • Gene Expression
  • Gene Expression Regulation, Bacterial
  • Lysogeny
  • Microbial Viability
  • Oligopeptides / physiology
  • SOS Response, Genetics*


  • DNA-Binding Proteins
  • Escherichia coli Proteins
  • MazE protein, E coli
  • MazF protein, E coli
  • Oligopeptides
  • asparagyl-aspargyl-tryptophyl-asparagyl-asparagine
  • Endoribonucleases

Grants and funding

This work was supported by the Israel Science Foundation (grant 66/10) and the United States Army (grant W911NF-09-1-0212). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.