Abstract
The multiple-antibiotic resistance (mar) locus (min 34) regulates a resistance to chloramphenicol in Escherichia coli that does not involve acetyltransferase. Transport studies showed that wild-type cells had an apparent endogenous active efflux of chloramphenicol which depended on the proton motive force. This efflux was not altered by a 39-kb chromosomal deletion which included the mar locus. Nevertheless, mutations at the mar locus led to a stronger net chloramphenicol efflux. Therefore, a gene encoding the putative efflux system cannot be at the mar locus but may be positively influenced by that locus.
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