Min Of Infection Research Articles

Inhibition of host protein synthesis during infection of Escherichia coli by bacteriophage T4. I. Continued synthesis of host ribonucleic acid.

The ribonucleic acid (RNA) synthesized at specified intervals during infection of Escherichia coli K-12 by bacteriophage T4 was hybridized to denatured E. coli or T4 deoxyribonucleic acids (DNA). The reactions were performed under conditions that maximized the yield and at RNA/DNA inputs such that excess DNA sites were available for all RNA species. Most of the RNA synthesized at any time during the first 3 min of infection was host-specific. The fraction declined rapidly as infection progressed; host RNA represented about half that made between 3 and 4 min. It is unlikely that this represented RNA synthesized by bacteria that had escaped infection, as judged by the kinetics of adsorption and killing as well as by the rapid inhibition of beta-galactosidase induction after infection. The nature of the host RNA was also examined. Part of the RNA synthesized during infection of cells rendered sensitive to actinomycin was stable in the presence of this inhibitor. This RNA was essentially all host-specific and it sedimented as ribosomal and transfer RNA; most of the ribosomal RNA was incorporated into 30S and 50S ribosomes. Hybridization analyses suggested that unstable E. coli messenger RNA was also synthesized for several minutes after infection; the proportion of unstable to stable host RNA synthesized appeared to be similar in infected and uninfected cells. Thus, it is concluded that significant amounts of E. coli RNA are synthesized during the first minutes of T4 infection. Host messenger RNA initiated after infection may not be translated into enzymes; alternatively, it is conceivable that continued bacterial messenger RNA synthesis only reflects the completion of transcription of operons whose reading was initiated prior to infection.

Bacteriophages Attacking an L-Glutamic Acid-Producing Strain of Microbacterium ammoniaphilum

Inhibitory action of sodium tripolyphosphate (Na-TPP) to P-phages growth was studied. Na-TPP had no phagicidal action, did not prevent adsorption of phage and inhibited for-mation of infected cells. Furthermore, no phase yield occurred when Na-TPP was added within 5 min of infection, but addition after that time resulted in normal phage growth. DNA synthesis of infected cells was blocked by Na-TPP added early in the latent period (within 5 min), but addition after that time failed to block its synthesis. RNA synthesis of infected cells was not affected even when Na-TPP was added at various times in the latent period. Furthermore, 72 per cent of 32P-labeled phage P-1 adsorbed in the medium containing Na-TPP was separated by the blendor treatment, but only 12 per cent was separated when adsorbed in the absence of Na-TPP. These results indicate that Na-TPP inhibits the injection of phage DNA into the host cell.

Bacteriophages Attacking an L-Glutamic Acid-Producing Strain of Microbacterium ammoniaphilum

Inhibitory action of sodium tripolyphosphate (Na-TPP) to P-phages growth was studied. Na-TPP had no phagicidal action, did not prevent adsorption of phage and inhibited for-mation of infected cells. Furthermore, no phase yield occurred when Na-TPP was added within 5 min of infection, but addition after that time resulted in normal phage growth. DNA synthesis of infected cells was blocked by Na-TPP added early in the latent period (within 5 min), but addition after that time failed to block its synthesis. RNA synthesis of infected cells was not affected even when Na-TPP was added at various times in the latent period. Furthermore, 72 per cent of 32P-labeled phage P-1 adsorbed in the medium containing Na-TPP was separated by the blendor treatment, but only 12 per cent was separated when adsorbed in the absence of Na-TPP. These results indicate that Na-TPP inhibits the injection of phage DNA into the host cell.