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DNA polymerase I-dependent mutants of coliphage lambda.

H Shizuya, D Brown, A Campbell

Journal of Virology

|May 1, 1974

Summary

Bacteriophage lambda mutants unable to grow on DNA polymerase I-deficient hosts were identified. These mutants, including recombination-deficient (red(-)) strains, exhibit severe growth defects on these hosts, revealing new genetic interactions.

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Area of Science:

Molecular Biology
Virology
Genetics

Background:

Bacteriophage lambda is a model system for studying viral replication and genetics.
DNA polymerase I (polA) plays a crucial role in DNA replication and repair.
Previous studies identified recombination (red) and ג€gamג€ (gam) genes in lambda phage.

Purpose of the Study:

To identify bacteriophage lambda mutants that cannot infect or replicate in hosts lacking DNA polymerase I (polA(-)).
To characterize the genetic basis of these plating defects and understand the role of lambda genes in polA(-) hosts.

Main Methods:

Mutagenesis of bacteriophage lambda.
Screening for mutants unable to plate on polA(-) bacterial hosts.
Characterization of mutant phenotypes, including burst size and lysis timing.
Genetic analysis to identify mutations and map their locations.

Main Results:

Mutants unable to plate on polA(-) hosts were predominantly recombination-deficient (red(-)).
red(-) and gam(-) mutants showed significantly reduced burst sizes and delayed lysis in polA(-) hosts compared to wild-type lambda.
Lambda mutants lacking red and gam expression (lambdaN(-)nin, lambdabio) also failed to plate on polA(-) hosts.
Bypass mutations (pas) were identified in lambda bio mutants that restored plating on polA(-) hosts.

Conclusions:

The red and gam genes of bacteriophage lambda are essential for efficient growth in DNA polymerase I-deficient hosts.
Lambda phage requires specific genes to overcome host DNA replication or repair deficiencies.
A novel bypass mutation (pas) has been identified, providing new insights into lambdaג€™s interaction with host DNA metabolism.

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