[Exchange of putrescine and potassium between cells and media as a factor in the adaptation of Escherichia coli to hyperosmotic shock].

Putrescine/potassium exchange in response to hyperosmotic stress was studied. The addition of 0.3 M NaCl or 0.44 M sucrose to an exponentially growing E. coli culture induced potassium uptake and putrescine release from the cell. Potassium added to an osmotically stressed potassium-deficient culture was readily absorbed by cells; this was accompanied by the loss of intracellular putrescine, both free and bound. Since DNA is the main binding site of putrescine, the loss of bound putrescine caused a relaxation of DNA supercoiling. The increase in the intracellular content of potassium not only restored but also enhanced DNA supercoiling as compared to the initial level. In vitro experiments showed the degree of plasmid DNA supercoiling to rise drastically at potassium concentrations of 300-500 mM, while different putrescine concentrations affected this parameter differently. Thus, the physiological concentrations of putrescine (below 1 mM) greatly augmented DNA supercoiling, whereas higher concentrations (5-10 mM) exerted a relaxing effect. A change in DNA supercoiling in vivo in response to osmotic stress is the result of competition between biogenic and abiogenic cations for the sites of binding to polyanionic DNA structures. A change in DNA topology serves as the regulatory factor controlling the expression of genes responsible for cell adaptation to osmotic stress.