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Shiga-toxin-converting bacteriophages.

H Schmidt1

  • 1Institut für Hygiene und Mikrobiologie der Universität Würzburg, Germany. hschmidt@hygiene.uni-wuerzburg.de

Research in Microbiology
|November 1, 2001
PubMed
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Shiga toxins (Stx), potent cytotoxins causing severe human disease, are primarily produced by Escherichia coli and Shigella dysenteriae. Stx-converting bacteriophages (Stx phages) play a crucial role in Stx expression and gene transfer, contributing to new STEC variants.

Area of Science:

  • Microbiology
  • Bacteriology
  • Genetics

Background:

  • Shiga toxins (Stx) are potent cytotoxins responsible for severe human diseases.
  • Stx are primarily produced by Escherichia coli and Shigella dysenteriae type 1.
  • The genes encoding Stx are typically found within the genomes of lambdoid prophages, known as Stx-converting bacteriophages (Stx phages).

Purpose of the Study:

  • To investigate the role of Stx-converting bacteriophages in the expression and dissemination of Shiga toxins.
  • To understand the genetic location and regulatory mechanisms controlling Stx production.
  • To elucidate the contribution of Stx phages to the emergence of new Shiga toxin-producing E. coli (STEC) variants.

Main Methods:

  • Bioinformatic analysis of Stx phage genomes.

Related Experiment Videos

  • Gene expression studies focusing on the late region of the phage genome.
  • Investigation of phage induction and transduction processes.
  • Main Results:

    • Stx genes are located in a conserved position within the late region of Stx phage genomes, downstream of the PR' promoter.
    • The location suggests regulation by a Q-like antiterminator, implying phage induction triggers Stx production.
    • Stx phages are capable of in vivo and in vitro transduction, facilitating lateral gene transfer.

    Conclusions:

    • Stx phages are critical for Shiga toxin expression and dissemination.
    • Phage induction is a key event in activating Stx production.
    • Stx phages significantly contribute to the emergence and evolution of STEC through lateral gene transfer.