Abstract
Chronic exposure of E. coli to ethanol during growth resulted in major changes in lipid composition. These ethanol-induced changes, a decrease in the proportion of saturated fatty acids, are similar to those which occur following a shift to lower temperature. Products of ethanol metabolism such as acetaldehyde and acetate caused the opposite changes in fatty acid composition. In vivo studies using mutants blocked in lipid synthesis indicated that saturated fatty acid synthesis was the primary target leading to changes in bulk lipid fatty acid composition. This was confirmed in vitro and condensing enzyme II was identified as the probable site of ethanol inhibition. The acute affects of ethanol on the function of two membrane-bound enzymes, Mg++ATPase and lac permease were also examined. In both cases, cells grown in the presence of ethanol. In time-course studies, permease function was restored concurrently with changes in lipid composition. Mutants were isolated which were able to grow in the presence of high levels of ethanol. These mutants displayed exaggerated changes in lipid composition providing evidence that alcohol-resistance and fatty acid changes are related.
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