McMurry L M, George A M, Levy S B
Center for Adaptation Genetics and Drug Resistance, Tufts University School of Medicine, Boston, Massachusetts 02111.
Antimicrob Agents Chemother. 1994 Mar;38(3):542-6. doi: 10.1128/AAC.38.3.542.
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.
多重抗生素耐药性（mar）位点（最小34）调控大肠杆菌中对氯霉素的耐药性，该耐药性不涉及乙酰转移酶。转运研究表明，野生型细胞存在明显的氯霉素内源性主动外排，这依赖于质子动力势。这种外排在包含mar位点的39 kb染色体缺失时并未改变。然而，mar位点的突变导致更强的氯霉素净外排。因此，编码假定外排系统的基因不在mar位点，但可能受到该位点的正向影响。
