Effect of infection with T-even phage on the inducible synthesis of β-galactosidase in Escherichia coli

The induction of β-d-galactosidase in Escherichia coli is inhibited promptly upon infection with T-even bacteriophage. This inhibition does not require phage-specific protein synthesis. When a pre-induced culture is infected, its capacity to form β-galactosidase decays exponentially after a brief delay. In cells carrying the F episome (F⁺, Hfr or F lac), this decay of enzyme-forming capacity proceeds at the same rate, whether induction is arrested by phage infection or by inducer removal. On the other hand, in F^- strains the rate of decay after phage infection is twice as fast as after inducer removal. No differences in phage development are detectable in F⁺ and F^- strains. Irradiation of the phage particles with small doses of ultraviolet light, insufficient to affect the production of early phage enzymes, completely abolishes the effect of phage on the decay of β-galactosidase-forming capacity. Therefore, the ability to accelerate the breakdown may reside in the genetic material of the virus. This phage function is repressed by the F episome of the host.