THEORETICAL MECHANISMS OF DIFFERENTIATION.
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Biomedical subjects
Publications and source records attributed to B D DAVIS.
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Brief treatment of growing Escherichia coli with penicillin hastened subsequent killing of these cells by streptomycin. It also hastened the secondary uptake of streptomycin, which represents an increase in the number of freely accessible binding sites. In contrast, brief treatment with streptomycin failed to affect subsequent killing by penicillin. These findings suggest that the synergism of penicillin with streptomycin depends on the damaging effect of penicillin on the cell membrane, which promotes further damage by streptomycin and increases its subsequent access to intracellular sites. Observations on a streptomycin-resistant mutant are also reported.
Plotz, Paul H. (Harvard Medical School, Boston, Mass.) and Bernard D. Davis. Absence of a chloramphenicol-insensitive phase of streptomycin action. J. Bacteriol. 83:802-805. 1962.-Previous findings have suggested the possibility that the damaging effect of streptomycin on the bacterial cell membrane is only preliminary to an intracellular lethal action. Since the membrane effect requires protein synthesis, a two-stage action might be recognized if the second stage did not require protein synthesis. Indeed, it has been reported that Escherichia coli cells, pretreated with streptomycin, are not protected by chloramphenicol from subsequent killing by streptomycin in a nitrogen-free medium. However, we were unable to confirm this report or to observe any chloramphenicol-insensitive phase of streptomycin action in a growth medium. It is, therefore, not yet possible to decide whether the lethal event occurs at the membrane or within the cell.
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