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Altered phenotypes associated with ampD mutations in Enterobacter cloacae.

G Korfmann1, C C Sanders, E S Moland

  • 1Department of Medical Microbiology, Creighton University School of Medicine, Omaha, Nebraska 68178.

Antimicrobial Agents and Chemotherapy
|February 1, 1991
PubMed
Summary
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The AmpC beta-lactamase induction in Enterobacter cloacae is regulated by the ampD gene. This gene encodes a protein crucial for sensing antibiotic inducers, influencing enzyme activity and bacterial resistance.

Area of Science:

  • Microbiology
  • Genetics
  • Molecular Biology

Background:

  • AmpC beta-lactamase is a key enzyme in Enterobacter cloacae conferring resistance to beta-lactam antibiotics.
  • Understanding the regulation of AmpC expression is crucial for combating antibiotic resistance.

Purpose of the Study:

  • To identify the genetic locus responsible for altered AmpC beta-lactamase expression in Enterobacter cloacae.
  • To investigate the role of the ampD gene in the induction of AmpC beta-lactamase.

Main Methods:

  • Cloning and transformation of the ampD region from various E. cloacae strains into an ampD mutant Escherichia coli strain.
  • Assessing AmpC beta-lactamase activity in sonic extracts of cells under different conditions (temperature, inducers).

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Main Results:

  • Altered AmpC expression phenotypes were localized to the ampD locus.
  • The ampD gene encodes a protein involved in sensing antibiotic inducers.
  • Temperature-sensitive ampD variants showed differential induction responses to cefotetan at varying temperatures.

Conclusions:

  • The ampD gene plays a significant role in the induction of AmpC beta-lactamase in Enterobacter cloacae.
  • The AmpD protein is likely involved in the sensing mechanism for beta-lactamase induction.