A colicin-tolerant mutant of Escherichia coli which is temperature-dependent for tolerance and unable to grow at 40° without the addition of salt, plates λ+ wild-type phage with a reduced frequency and very turbid plaques at 30°, failing to form any plaques at 40° even though the cells become phage infected. Phage mutants λcI, λcII, λcY42 and λvir form clear plaques and plate with equal efficiency on the mutant and its parent strain at both temperatures. The results show that over 95% of the phage infected cells become lysogenized after λ+ phage infection. In contrast, the temperate phage P1 formed normal turbid plaques with equal frequency on both bacterial strains, but phage ϕ80 forms normal turbid plaques at 30° and clear (non-lysogenic) plaques at 40°. An investigation of the mutant strain showed that it not only lacked a large molecular weight component from its cell envelope but also had reduced capacity to synthesize cyclic-3′,5′-AMP. It is proposed that the mutation(s) in the colicin-tolerant mutant gives rise to a number of alterations, one of which changes the cell envelope and leads to the reduction of intracellular cyclic AMP and the other giving rise to an altered RNA polymerase specificity. These alterations lead to a changed ratio of the products of the λ-genes involved in the control of lysogeny and give rise to a bias towards the lysogenic response. The cIII gene product of λ is not as essential to lysogeny as cII or cI and therefore possibly acts as an internal control of other λ functions (e.g. cro).