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Related Experiment Videos

Mutations in coliphage p1 affecting host cell lysis.

J T Walker1, D H Walker

  • 1Department of Microbiology, University of Iowa, Iowa City, Iowa 52242.

Journal of Virology
|August 1, 1980
PubMed
Summary
This summary is machine-generated.

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Investigating coliphage P1 amber mutants revealed defects in lysis and morphogenesis. Gene 10 mutants are unable to synthesize late proteins, suggesting a role in regulating gene expression for phage production.

Area of Science:

  • Bacteriophage genetics
  • Molecular biology
  • Microbial genetics

Background:

  • Bacteriophage P1 is a model system for studying viral replication and lysis.
  • Amber mutants are essential tools for dissecting essential viral genes.
  • Understanding phage lysis mechanisms is crucial for controlling viral infections.

Purpose of the Study:

  • To characterize the function of genes involved in coliphage P1 lysis and morphogenesis.
  • To identify genes essential for phage particle production and cell lysis.
  • To investigate potential regulators of late gene expression in coliphage P1.

Main Methods:

  • Analysis of 103 amber mutants of coliphage P1.
  • Testing lysis of nonpermissive cells.
  • Assessing phage particle production in artificially lysed cells.

Related Experiment Videos

  • Thin section electron microscopy of infected cells.

    • Main Results:

    • 83 mutants showed defects in particle morphogenesis.
    • 5 mutants (gene 2) caused premature lysis, suggesting a lysis regulator defect.
    • 15 mutants were unable to cause cell lysis.
    • 5 of the lysis-defective mutants (gene 17) had defects in lysis function, producing viable phage after artificial lysis.
    • 10 lysis-defective mutants (gene 10) could not produce viable phage, indicating a defect in late protein synthesis.

    Conclusions:

    • Coliphage P1 gene 17 is essential for lysis function.
    • Coliphage P1 gene 10 mutants are defective in late protein synthesis.
    • Gene 10 may regulate late gene expression in coliphage P1.