Interaction of host and viral regulatory mechanisms: Effect of the lon cell division defect on regulation of repression by bacteriophage lambda

The Escherichia coli lon cell division mutant, which is lysogenized with reduced frequency by λ and other lambdoid phages, produced only one-half the λ repressor activity found in lon⁺ cells after λ infection. A similar reduction of repressor level was observed in λcro-infected lon cells, compared to λcro-infected lon⁺ cells, indicating that the lon effect on repressor activity is not the result of an altered interaction with the λcro⁺ gene product. λ late gene functions were not efficiently shut off in λ⁺-infected lon cells, as demonstrated by elevated endolysin levels and phage yields. Although lon cells are lysogenized inefficiently, lon lysogens can be isolated and are stable. Mono-lysogens of lon⁺ and lon strains contained similar repressor levels. Thus, the lon defect results in reduced repressor activity during the establishment of repression, but not during maintenance of lysogeny. λ mutants (λtp) have been selected for the ability to form turbid plaques on lon hosts. After infection by λtp, repressor levels in both lon⁺ and lon cells were twofold higher than the levels in λ⁺-infected cells. Established lon⁺ and lon mono-lysogens of the λtp mutants contained repressor activity levels similar to those in λ⁺ mono-lysogens.