A novel plasmid gene involved in bacteriophage PRD1 infection and conjugative host-range

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High-Resolution Comparison of Bacterial Conjugation Frequencies
05:18

High-Resolution Comparison of Bacterial Conjugation Frequencies

Published on: January 10, 2019

M Holcík1, V N Iyer

  • 1Department of Biology, Carleton University, Ottawa, Ontario, Canada. mholcik@hhmivax.humgen.upenn.edu

Plasmid
|May 1, 1996
PubMed

Insights

Bacteriophage PRD1 resistance in bacteria with IncN plasmids is linked to mutations in the kikA locus. One kikA gene restores normal phage infection and bacterial conjugation, impacting host-phage interactions.

Area of Science:

  • Microbiology
  • Virology
  • Genetics

Background:

  • Bacteriophage PRD1 infects bacteria by attaching to conjugative pili, which are encoded by IncN plasmids.
  • The IncN plasmid locus kikA is located near the pilus region and influences PRD1 infection and bacterial conjugation.

Purpose of the Study:

  • To investigate the role of the kikA locus in PRD1 resistance and bacterial conjugation.
  • To determine which gene within kikA is responsible for restoring normal phenotypes.

Main Methods:

  • Analyzing mutations in the kikA locus of IncN plasmids.
  • Assessing PRD1 resistance and conjugation proficiency in modified bacteria (Klebsiella and Escherichia coli).
  • Evaluating the effect of individual kikA genes on bacterial phenotypes.

Main Results:

  • Mutations in kikA confer PRD1 resistance and reduce conjugation in Klebsiella but not E. coli.
  • One of the two kikA genes is sufficient to restore both PRD1 susceptibility and normal conjugation.
  • PRD1 binds to cells with mutant plasmids but cannot inject its genome, indicating a block in infection.

Conclusions:

  • The kikA locus plays a crucial role in mediating PRD1 infection and bacterial conjugation.
  • Specific genes within kikA are essential for host-bacteriophage interactions and plasmid transfer.
  • Understanding kikA function provides insights into phage resistance mechanisms and bacterial genetics.

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