Magnesium-dependent plaque formation by bacteriophage P1cinC(-) on Escherichia coli C and Shigella sonnei

Virology
|November 1, 1986
PubMed

Insights

Phage P1C(-) infects certain bacteria like E. coli C and Shigella sonnei, but not others. Its infectivity depends on bacterial lipopolysaccharide structure and Mg2+ presence.

Area of Science:

  • Bacteriology and Virology
  • Molecular Biology
  • Microbial Genetics

Background:

  • Bacteriophages are viruses that infect bacteria, playing roles in microbial evolution and gene transfer.
  • Phage P1 is a well-studied temperate bacteriophage with a broad host range, including Escherichia coli.
  • The infectivity of bacteriophages is often determined by specific receptors on the bacterial surface, such as lipopolysaccharides (LPS).

Purpose of the Study:

  • To investigate the host range and infectivity of a modified phage P1, designated P1C(-).
  • To determine the role of magnesium ions (Mg2+) in P1C(-) infection.
  • To explore the relationship between bacterial lipopolysaccharide structure and susceptibility to P1C(-) infection.

Main Methods:

  • Plaque assays were performed on various bacterial strains including Escherichia coli C, Shigella sonnei, Citrobacter freundii, Enterobacter aerogenes, Klebsiella pneumoniae, Proteus rettgeri, and Salmonella typhimurium mutants and wild-type strains.
  • Lysogenization experiments were conducted to assess the ability of P1C(-) to integrate into bacterial genomes.
  • The presence or absence of Mg2+ was controlled during infection experiments.
  • Analysis of lipopolysaccharide structure of susceptible and non-susceptible bacterial strains.

Main Results:

  • Phage P1C(-) formed plaques on Escherichia coli C and Shigella sonnei in the presence of Mg2+, indicating infectivity.
  • Citrobacter freundii, Enterobacter aerogenes, and a Salmonella typhimurium galE mutant were lysogenized by P1C(-) but not lysed.
  • Klebsiella pneumoniae, Proteus rettgeri, and Salmonella typhimurium LT2 were resistant to both P1C(-) and the wild-type P1C(+) phage.
  • Differences in lipopolysaccharide structure are implicated as key factors determining bacterial susceptibility to P1C(-) infection.

Conclusions:

  • Phage P1C(-) exhibits a distinct host range compared to wild-type P1, with infectivity influenced by Mg2+ and bacterial LPS.
  • The study highlights the critical role of bacterial surface structures, specifically LPS, in mediating bacteriophage tropism.
  • P1C(-) can act as a tool for studying LPS structure and phage-host interactions in Gram-negative bacteria.

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