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

Christine L. Truitt, William G. Haldenwang, James R. Walker

Research output: Contribution to journalArticlepeer-review

7 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)231-244
Number of pages14
JournalJournal of Molecular Biology
Volume105
Issue number2
DOIs
StatePublished - Aug 5 1976
Externally publishedYes

ASJC Scopus subject areas

  • Structural Biology
  • Molecular Biology

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