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Molecular characterization of the fragilysin pathogenicity islet of enterotoxigenic Bacteroides fragilis

J S Moncrief1, A J Duncan, R L Wright

  • 1Department of Biochemistry, Fralin Center for Biotechnology, Virginia Polytechnic Institute and State University, Blacksburg 24061-0346, USA. jmoncrie@vt.edu

Insights

Enterotoxigenic Bacteroides fragilis harbors the fragilysin gene on a mobile genetic element called the pathogenicity islet. This islet integrates into specific chromosomal sites, potentially influencing toxin production and bacterial virulence.

Area of Science:

  • Microbiology
  • Genetics
  • Molecular Biology

Background:

  • Enterotoxigenic Bacteroides fragilis produces fragilysin, a metalloprotease toxin.
  • Fragilysin causes intestinal epithelial cell damage, fluid secretion, and tissue injury.

Purpose of the Study:

  • To characterize the genetic element containing the fragilysin gene.
  • To investigate the integration mechanism of this genetic element in the Bacteroides fragilis chromosome.

Main Methods:

  • DNA sequencing of the fragilysin pathogenicity islet.
  • Polymerase Chain Reaction (PCR) analysis of multiple bacterial strains.
  • Chromosomal integration site analysis.

Main Results:

  • The fragilysin gene is located on a 6,033 bp genetic element, the fragilysin pathogenicity islet, flanked by direct repeats.
  • The islet integrates at a specific chromosomal locus in enterotoxigenic strains.
  • A distinct GC-rich sequence was identified at the integration site in non-toxigenic strains, suggesting it as a potential integration target.
  • An additional open reading frame encoding a putative protein similar to fragilysin was identified within the islet.

Conclusions:

  • The fragilysin pathogenicity islet is a mobile genetic element responsible for carrying the fragilysin gene.
  • Chromosomal integration of the islet occurs at a specific site, with non-toxigenic strains lacking a characteristic target sequence.
  • The presence of a second, similar gene suggests potential functional redundancy or evolution of the toxin system.

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