This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Winkler, H. H. Articles by Duckworth, D. H. Search for Related Content PubMed PubMed Citation Articles by Winkler, H. H. Articles by Duckworth, D. H.

Metabolism of T4 Bacteriophage Ghost-Infected Cells: Effect of Bacteriophage and Ghosts on the Uptake of Carbohydrates in Escherichia coli B

Department of Microbiology, University of Virginia School of Medicine, Charlottesville, Virginia 22903

ABSTRACT

Ghosts of T4 bacteriophage inhibit the uptake of thiomethyl-ß-galactoside (TMG), -methylglucoside, glucose-6-phosphate, and glycerol in Escherichia coli B. The transport of orthonitrophenyl-ß-galactoside (ONPG) is also inhibited to a lesser degree and without alteration of the apparent K_m of transport. These effects of ghosts parallel those of energy poisons on these systems. However, no one energy poison can produce such pronounced inhibitory effects in all these systems. The effect of the intact phage in these systems was either absent or very slight relative to the ghost. The effect of ghosts on the uptake of TMG was not immediate; at 10 C, no effect of the ghosts was apparent for at least 2 min. This suggests that a step, more temperature dependent than the attachment of the ghost, is necessary for the inhibitory action. The intracellular level of adenosine triphosphate (ATP) in the ghost-infected cells fell to less than 25% of the control value, and the ATP lost from the cell appeared in extracellular medium. Phage, on the other hand, caused no decrease in the intracellular ATP level. This loss of ATP from the cells after ghost infection suggests an alteration of the barrier properties of the membrane so that ATP can leave the cell; however, the accessibility of extracellular ONPG to intracellular ß-galactosidase does not increase. The dissimilarity of the actions of phage and ghosts on all properties examined does not support the model that the initial events in their infections are identical but that the intact phage, unlike the ghost, can provide information for the repair of its effects.