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Published on: May 6, 2018
Magnesium-dependent plaque formation by bacteriophage P1cinC(-) on Escherichia coli C and Shigella sonnei
Abstract:
Phage P1C(-), in a state of the phage not infective to Escherichia coli K12, was able to form plaques on a wild-type strain of E. coli C and on Shigella sonnei in the presence of Mg2+. Citrobacter freundii, Enterobacter aerogenes, and a Salmonella typhimurium galE mutant were not lysed by, but were lysogenized with P1cinC(-), whereas Klebsiella pneumoniae, Proteus rettgeri, and S. typhimurium LT2 were not susceptible to either P1cinC(-) or P1cinC(+). The lipopolysaccharide structure of E. coli C and Sh. sonnei is discussed with reference to receptors for P1cinC(-) and P1cinC(+).
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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