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- Title
The Bacteriophage Lambda CII Phenotypes for Complementation, Cellular Toxicity and Replication Inhibition Are Suppressed in cII-oop Constructs Expressing the Small RNA OOP.
- Authors
Rajamanickam, Karthic; Hayes, Sidney
- Abstract
The temperate bacteriophage lambda (λ) CII protein is a positive regulator of transcription from promoter pE, a component of the lysogenic response. The expression of cII was examined in vectors devoid of phage transcription-modulating elements. Their removal enabled evaluating if the expression of the small RNA OOP, on its own, could suppress CII activities, including complementing for a lysogenic response, cell toxicity and causing rapid cellular loss of ColE1 plasmids. The results confirm that OOP RNA expression from the genetic element pO-oop-to can prevent the ability of plasmid-encoded CII to complement for a lysogenic response, suggesting that it serves as a powerful regulatory pivot in λ development. Plasmids with a pO promoter sequence of 45 nucleotides (pO45), containing the -10 and -35 regions for oop, were non-functional; whereas, plasmids with pO94 prevented CII complementation, CII-dependent plasmid loss and suppressed CII toxicity, suggesting the pO promoter has an extended DNA sequence. All three CII activities were eliminated by the deletion of the COOH-terminal 20 amino acids of CII. Host mutations in the hflA locus, in pcnB and in rpoB influenced CII activities. These studies suggest that the COOH-terminal end of CII likely interacts with the β-subunit of RNA polymerase.
- Subjects
BACTERIOPHAGE lambda; CELL-mediated cytotoxicity; LYSOGENIC immunity; GENETIC transcription; PLASMIDS; THERAPEUTICS
- Publication
Viruses (1999-4915), 2018, Vol 10, Issue 3, p115
- ISSN
1999-4915
- Publication type
Article
- DOI
10.3390/v10030115