Reproduction of bacteriophage T6 and T7 in auxotrophic mutants ofE. coli B

Summary Phage T₆ and T₇ did not reproduce in mutants ofE. coli auxotrophic for the amino acids methionine, leucine, serine, proline, histidine, tyrosine, phenylalanine and tryptophane unless these amino acids were present in the medium. Very small amounts of these auxotrophic factors (0.01 γ/ml) are able to support phage multiplication. Much care has to be taken to avoid impurities in the medium and to deplete the endogenous reserves of the host cells.     

Inactivation of receptors for bacteriophage T5 during infection of Escherichia coli B.

During infection of Escherichia coli by bacteriophage T5, the cell surface receptors for the phage were inactivated so that they could not be isolated from the infected cells. A mutant of T5 that could only inject 8% of the T5 DNA did not cause the inactivation.     

Biological consequences of infection of Escherichia coli B by alkylated T7 bacteriophage.

Alkylation of T7 bacteriophage considerably delayed phage development and reduced the phage's killing action on host cells. Only a small fraction of infected cells produced phage. For these phages, the latent period was markedly prolonged but the burst was equivalent to or only slightly lower than that of untreated phage. In the progeny of alkylated phage, there was an increase in the fraction of defective particles as well as a change in their morphology. These data show that infection with alkylated T7 bacteriophage is to a large degree abortive; hence, biological consequences of this infection are very different from those characteristic of a normal virus infection.     

Bacteriophage Tail Components IV. Pteroyl Polyglutamate Synthesis in T4D-Infected Escherichia coli B

The nature of pteroyl polyglutamates in uninfected and T4D bacteriophage-infected Escherichia coli B has been examined. (3)H-p-aminobenzoic acid has been used to label the folate compounds and gel permeation chromatography on glass beads to separate the folate compound by molecular size. It has been found that, although the major folate compound in uninfected bacteria is pteroyl triglutamate, E. coli B cells also contain folate compounds having as many as six glutamate residues. Infection with T4D stimulated the addition of glutamate residues to the lower-molecular-weight host pteroyl compounds, resulting in the conversion of the host compounds into the hexaglutamate form. This viral-induced conversion is chloramphenicol sensitive and appears to be due to a late phage gene product. The phage gene responsible for this conversion has not been identified. In cells infected with a T4D mutant defective in gene 28, there was an apparent production of the large pteroyl polyglutamates equivalent in size to pte(glu)(9-12). These high-molecular-weight forms were converted into pte(glu)(6) by incubation with bacterial extracts made after infection with T4D 28(+). Apparently, the product of T4D gene 28(+) is capable of specifically cleaving the high-molecular-weight polyglutamates to the form necessary for phage tail assembly.     

The protein coats or ghosts or coliphage T2. III. Metabolic studies of Escherichia coli B infected with T2 bacteriophage ghosts

Assimilation of oxygen, inorganic phosphate, and ammonia nitrogen by normal T2 phage and T2 ghost-infected E. coli B was studied. The rate of oxygen and phosphorus uptake by ghost-infected bacteria is similar to that of normal and phage-infected cells. The R.Q. in glucose-salts medium remains approximately 1. Assimilation of ammonia nitrogen by ghost-infected bacteria is maintained at a rate approximately 80 per cent of normal. The inorganic phosphate which is assimilated was found to be incorporated into TCA-soluble compounds which were rapidly released into the medium. Within 5 minutes after absorption of the ghosts there was a loss from the cell of TCA-soluble constituents including organic phosphorus and compounds which absorb at 260 mmicro. No corresponding breakdown of nucleic acid present in the cell prior to infection could be detected. The incorporation of inorganic phosphate into organic linkages in the ghost-infected cell and its release into the medium were found to proceed at a rate approaching that of the incorporation of inorganic phosphorus into the nucleic acid of normal cells. The net increase in 260 mmicro absorbing compounds appeared to be inhibited.