The Role of Recombination in Growth of Bacteriophage Lambda II. Inhibition of Growth by Prophage P2

Abstract

In this series we are investigating the role of recombination in the growth of bacteriophage λ. In the preceding paper we described a new λ gene called γ (gamma). γ⁻ mutants are slightly deficient in repair of UV damage (in recA⁻ hosts) and also in recombination. Like recombination-deficient (red⁻) mutants, γ⁻ mutants do not form plaques on certain strains of Escherichia coli (among which are E. coli mutants deficient in DNA polymerase). Phages that are both red⁻ and γ⁻ do not form plaques on recA⁻ strains of E. coli, possibly because of cumulative adverse effects of the two mutations on growth. Failure to form plaques on recA⁻ is called the fec⁻ phenotype (Manly et al., 1969).

Wild-type λ does not form plaques on lysogens carrying the unrelated phage P2 (Lederberg, 1957), and is therefore said to be spi⁺ (sensitive to P2 interference). Lindahl et al. (1970), who studied this phenomenon, described spi⁻ mutants of λ that can form plaques on P2 lysogens. They concluded that the spi⁻ phenotype required inactivation of at least two λ genes: one gene maps under the bio72 deletion; another maps between the ends of the bio72 and bio1 deletions. They also found that the spi⁻ mutants they studied are fec⁻.

We show here that the combination red⁻γ⁻, which is sufficient for the fec⁻ phenotype, gives only a partial spi⁻ phenotype. The full spi⁻ phenotype requires in addition, the mutation of a new gene called δ (delta), located between int and exo. The δ⁻ mutation does...