Abstract
In the interaction between Escherichia coli virus T1 and its host cell, which leads to reorientation of macromolecule synthesis, the alteration of the host cell membrane is an important step: The proton-motive force is rapidly reduced. This became apparent from selective changes in energy-coupled transports: proton-motive force- and ATP-dependent transports are inhibited in wild type cells. However, in ATPase-deficient (unc-) cells the ATP-driven transports are not affected by T1. The membrane potential is reduced by T1 as was measured by triphenylmethylphosphonium ion distribution. The potassium gradient is dissipated and calcium ions are accumulated by the cells. However, the residual (but reduced) membrane energy is essential for T1 development since the addition of uncouplers prevents any viral production. Consistently, the cell membrane remains intact after T1 infection: proteins, like beta-galactoside, amino acids, and alpha-methylglucoside cannot passively penetrate the membrane of T1-infected cells.
Highlights
Its host cell, which leads to reorientation of macromolecule synthesis, the alteration of the host cell membrane is animportant step: The proton-motive force is rapidly reduced
The cell membrane remains intact after T1 infection: proteins, like 8-galactosidase, and small molecules, like
T h e inhibition of proline uptake was independent ona functioning ATPase, since ATPase-deficient E . coli were affected by T1 (Fig. lA).In contrast,in these unc- cells the rate of ATPdependent glutamine uptake was not or little affected by T 1 infection, whereas in the presence of a functioning ATPase glutamine uptake was inhibite(Fdig. 1B).These results indicated,that T1 infectiondissipated the electrochemical proton gradient of the cell membrane
Summary
Its host cell, which leads to reorientation of macromolecule synthesis, the alteration of the host cell. In ATPase-deficient (unc-) cells the ATP-driven transports are not affected by T1. The membrane potential is reduced by T1 as was measured by triphenylmethylphosphonium ion distribution. The cell membrane remains intact after T1 infection: proteins, like 8-galactosidase, and small molecules, like
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