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Temporal control of colicin E1 induction.

B Salles1, J M Weisemann, G M Weinstock

  • 1Department of Biochemistry and Molecular Biology, University of Texas Medical School, Houston 77057.

Journal of Bacteriology
|November 1, 1987
PubMed
Summary
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The colicin E1 gene (cea) in Escherichia coli is induced by DNA damage via the SOS response, but with a unique delay. Catabolite repression influences this induction, suggesting a complex regulatory mechanism for cea expression.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Colicin E1 (cea) is an antibiotic produced by Escherichia coli.
  • Its expression is regulated by complex cellular mechanisms.

Purpose of the Study:

  • To investigate the regulation of colicin E1 (cea) gene expression in Escherichia coli.
  • To understand the role of DNA damage, SOS response, and catabolite repression in cea regulation.

Main Methods:

  • Utilized cea-lacZ gene fusions in Escherichia coli.
  • Analyzed gene expression under various conditions, including DNA-damaging treatments and catabolite repression.

Main Results:

  • cea expression is induced by DNA damage and regulated by the SOS response.

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  • Expression exhibits a low basal level and sensitivity to catabolite repression.
  • Induction requires higher DNA damage levels and shows a pronounced delay compared to other SOS genes.
  • Catabolite repression exacerbates the delay in cea expression.

    • Conclusions:

    • The SOS response and catabolite repression systems intricately control cea expression.
    • The observed delay and regulatory nuances suggest a specific biological role for this regulation.