Bina Xiaowen, Perreten Vincent, Levy Stuart B
Center for Adaptation Genetics and Drug Resistance, Tufts University School of Medicine, Boston, Massachusetts 02111, USA.
J Bacteriol. 2003 Feb;185(4):1465-9. doi: 10.1128/JB.185.4.1465-1469.2003.
Escherichia coli strain TP985, which has an insertional mutation in the gene for the periplasmic murein tripeptide binding protein MppA, was previously reported to overproduce MarA and exhibit a multiple-antibiotic resistance (Mar) phenotype (H. Li and J. T. Park, J. Bacteriol. 181:4842-4847, 1999). We found that TP985 contained a previously unrecognized marR mutation which was responsible for the Mar phenotype. Transduction of the mppA mutation from TP985 to another wild-type strain did not affect antibiotic susceptibility. Overproduction of MppA repressed marA transcription in TP985 but not in other mppA or marR mutants. Therefore, TP985 contains an additional unknown mutation(s) that facilitates the repression of marA expression by MppA.
大肠杆菌菌株TP985在周质胞壁质三肽结合蛋白MppA的基因中存在插入突变,此前有报道称该菌株过量产生MarA并表现出多重抗生素耐药(Mar)表型(H. Li和J. T. Park,《细菌学杂志》181:4842 - 4847,1999年)。我们发现TP985含有一个先前未被识别的marR突变,该突变导致了Mar表型。将TP985的mppA突变转导至另一个野生型菌株并不影响抗生素敏感性。在TP985中过量表达MppA可抑制marA转录,但在其他mppA或marR突变体中则不然。因此,TP985含有另外一个未知突变,该突变有助于MppA对marA表达的抑制作用。