Phleomycin-stimulated solubilization of deoxyribonucleic acid in Escherichia coli. II. Inhibition of solubilization by bacteriophage T4

1976 ◽  
Vol 22 (5) ◽  
pp. 645-653 ◽  
Author(s):  
Larry D. Farrell ◽  
Harvard Reiter
Keyword(s):  
Escherichia Coli ◽  
Protein Synthesis ◽  
Deoxyribonucleic Acid ◽  
Cytoplasmic Membrane ◽  
Bacteriophage T4 ◽  
Continuous Exposure ◽  
Dna Endonuclease ◽  
Molecular Weights ◽  
Dependent Inhibition ◽  
Antibiotic Inhibition

Phleomycin-stimulated solubilization of Escherichia coli DNA is inhibited by infecting the cells with mutants of bacteriophage T4 before treatment with the antibiotic, inhibition requiring phage-specified protein synthesis. Two different modes of inhibition can be differentiated by infecting with mutants which are defective in an early state (gene den A−; endonuclease II-independent inhibition) or a late stage (gene 46−; endonuclease II-dependent inhibition) of phage-directed degradation of host DNA. Endonuclease II-independent inhibition results from interference with phleomycin-induced release of host DNA from the cytoplasmic membrane. In the presence of endonuclease II, the host DNA is converted to fragments, with average molecular weights of 106 daltons, the further degradation of which is not promoted by continuous exposure of the cells to phleomycin.

scholarly journals The Action of Bacteriophage Ω8 on Two Strains of Escherichia coli 08

Microbiology ◽  
2000 ◽  
Vol 81 (1) ◽  
pp. 131-144 ◽  
Author(s):  
Barbara Wallenfels ◽  
K. Jann
Keyword(s):  
Escherichia Coli ◽  
Protein Synthesis ◽  
Phage Particle ◽  
Cytoplasmic Membrane ◽  
Cellular Respiration ◽  
Bacterial Strains ◽  
Viral Dna ◽  
Killing Effect ◽  
E Coli ◽  
Phage Propagation

Bacteriophage Ω8 is propagated in Escherichia coli E56b (08: K27-:H-), a non-capsulated strain. Another non-capsulated strain, E. coli 2398 (08:K?-:H-), is killed by bacteriophage Ω8 without phage propagation. This strain was formerly believed to be E. coli 093:K?-:H-, cross-reacting with strain E56b. We have established chemical and serological identity of the 08-specific lipopolysaccharides of the two strains. The 08-specific lipopolysaccharides of both strains inhibited the infection of Escherichia coli E56b with bacteriophage Ω8 equally well. The adsorption rate constants of Ω8 were identical for the two strains of E. coli 08. Evidence was obtained with 32P-labelled bacteriophage Ω8 for penetration of viral DNA into both bacterial strains. In host strain E56b, phage particle synthesis occurred normally. In strain 2398 the viral DNA was not degraded but its expression was blocked. The killing effect of Ω8 on E. coli strain 2398 is supposed to be due to damage of the cytoplasmic membrane, which could not be reversed under the influence of viral information. This was indicated by a blockage of cellular respiration, β-galactoside transport and RNA as well as protein synthesis.

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