SUMMARY: The mutation in K12, which inactivates enterochelin esterase, allows the cell to accumulate ferric enterochelin. The ferric complex of enterochelin was released in significant quantities from a mutant after osmotic shock. Analysis of the effects of the individual stages of the shock procedure in wild-type cells showed that prior exposure of cells to sucrose and EDTA was not required, careful dilution of cells into a hypo-osmolar medium being sufficient to induce efflux of Fe. Prior treatment with EDTA or exposure to shearing forces served either to enhance efflux or to induce efflux in isotonic media. Neither vitamin B nor 5′-nucleotidase was released from the periplasm by these procedures. The release observed under mild conditions was stimulated specifically by Co, did not occur at 0 °C, and was inhibited by 2,4-dinitrophenol at 37 °C. From these observations, it was concluded that the efflux of Fe represents a physiological response of the cell to exposure to a hypo-osmolar medium. Such changes may enhance survival following physicochemical stressing of the bacterial outer membrane.


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