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Attaching and effacing locus of a Citrobacter freundii biotype that causes transmissible murine colonic hyperplasia

D B Schauer1, S Falkow

  • 1Department of Microbiology and Immunology, Stanford University School of Medicine, California 94305-5402.

Insights

Citrobacter freundii biotype 4280 causes attaching and effacing (AE) lesions in mice, similar to human enteropathogenic E. coli. This strain possesses a homologous eae gene essential for AE activity and disease development.

Area of Science:

  • Microbiology
  • Pathogenesis
  • Molecular Biology

Background:

  • Citrobacter freundii biotype 4280 induces transmissible murine colonic hyperplasia.
  • Attaching and effacing (AE) lesions are characteristic of this condition.
  • AE lesions are also caused by human enteropathogenic Escherichia coli.

Purpose of the Study:

  • To investigate the genetic basis of AE lesion formation by Citrobacter freundii biotype 4280.
  • To identify homologous genes to the E. coli eae gene in C. freundii.
  • To elucidate the role of the eae homolog in the pathogenesis of murine colonic hyperplasia.

Main Methods:

  • Southern blot analysis to detect DNA homology.
  • Cloning of the C. freundii eae homolog.
  • Nucleotide sequencing of the cloned gene.

Main Results:

  • Citrobacter freundii biotype 4280 contains DNA homologous to the eae gene, unlike 20 other C. freundii strains.
  • The eae homolog was successfully cloned and its nucleotide sequence determined.
  • The presence of the eae locus is linked to AE activity in C. freundii biotype 4280.

Conclusions:

  • The eae locus in Citrobacter freundii biotype 4280 is necessary for AE activity.
  • This eae homolog plays a role in the pathogenesis of transmissible murine colonic hyperplasia.
  • Findings suggest conserved mechanisms of AE lesion formation across bacterial species.

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