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PubMed1968

Cation fluxes and permeability changes accompanying bacteriophage infection of Escherichia coli.

Infection of Escherichia coli by bacteriophage T2 was accompanied by a rapid but transient increase in the rate of loss of small molecules from the bacterial cells. This transient leakage was studied with radioactive labels such as (42)K and (28)Mg. Bacteriophage-induced leakage was dependent on the ratio of phage to bacteria: the higher the multiplicity of infection, the greater the leakage. No leakage occurred at 4 C [when adsorption proceeds but injection of phage deoxyribonucleic acid (DNA) is blocked]. Leakage was caused by heavily irradiated phage as well as by normal phage; therefore, the intracellular functioning of the bacteriophage DNA was not required. This conclusion was supported by experiments which showed phage-induced leakage in the presence of chloramphenicol or sodium cyanide. Leakage could be prevented by infecting the bacteria with phage in the presence of high magnesium concentrations. Phage-induced leakage was terminated by a "sealing" reaction, after which potassium turnover by infected and uninfected cells was very similar. The sealing reaction occurred even in the presence of chloramphenicol, suggesting that the sealing is controlled by bacterial and not bacteriophage genes. We were not able to detect any effect of normal bacteriophage infection on the influx (active transport) of potassium and magnesium into the cells.

Adsorption↗
PubMed1963

POTASSIUM FLUXES IN DESHEATHED FROG SCIATIC NERVE.

Desheathed frog (R. pipiens) sciatic nerves were soaked in Na-deficient solutions, and measurements were made of their Na and K contents and of the movements of K(42). When a nerve is in Ringer's solution, the Na fluxes are equal to the K fluxes, and about 75 per cent of the K influx is due to active transport. The Na content and the Na efflux are linearly related to the Na concentration of the bathing solution, while the K content and the K fluxes are not so related. When a nerve is in a solution in which 75 per cent of the NaCl has been replaced by choline chloride or sucrose, the active K influx exceeds the active Na efflux, and the K content is maintained. When a nerve is soaked in a solution that contains Li, the K(42) uptake is inhibited, and the nerve loses K and gains Li. When a Li-loaded nerve recovers in a Li-free solution, K is taken up in exchange for Li. This uptake of K requires Na in the external solution. It is concluded that the active transports of K and of Na may be due to different processes, that an accumulation of K occurs only in exchange for an intracellular cation, which need not be Na, and that Na plays a specific, but unknown, role in K transport.

Animals↗