We have examined the effect of growth temperature on three systems normally induced under conditions of iron limitation: synthesis of the siderophore enterochelin (enterobactin), transport of ferric enterochelin, and production of the outer membrane protein which serves as the colicin I receptor. We found that although Salmonella typhimurium produces less enterochelin when grown at 42 degrees C, synthesis of this siderophore was not diminished in Escherichia coli grown under the same conditions. Growth at 42 degrees C under a condition of iron stress led to a reduction in the ability of cells to transport ferric enterochelin in both organisms. A two- to threefold decrease in the number of colicin I receptors was observed in cells of E. coli or S. typhimurium grown at 42 degrees C as compared with the number of receptors observed in cells grown at 37 degrees C. The colicin I receptor was shown not to be inherently unstable at 42 degrees C. By using a cir-lacZ operon fusion, it was shown that at least part of the decrease in receptor levels found in cells grown at high temperature was the result of decreased transcription of cir, the receptor structural gene. The effect of growth temperature on these systems was shown to be independent of fur, a regulatory element which mediates their enhanced production in response to iron stress. We suggest that a second regulatory element common to gene products involved in iron sequestration may be responsible for temperature regulation of these systems
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