SOS Regulation of qnrB Expression

被引：53

作者：

Wang, Minghua ^{[1
,2
]}

Jacoby, George A. ^{[3
]}

Mills, Debra M. ^{[3
]}

Hooper, David C. ^{[1
]}

机构：

[1] Massachusetts Gen Hosp, Boston, MA 02114 USA

[2] Fudan Univ, Inst Antibiot, Huashan Hosp, Shanghai 200433, Peoples R China

[3] Lahey Clin Fdn, Burlington, MA USA

来源：

ANTIMICROBIAL AGENTS AND CHEMOTHERAPY | 2009年 / 53卷 / 02期

基金：

美国国家卫生研究院;

关键词：

QUINOLONE RESISTANCE; ESCHERICHIA-COLI; GENE-EXPRESSION; PLASMID; MUTAGENESIS; MUTATIONS; INDUCTION;

D O I：

10.1128/AAC.00132-08

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

In the sequence upstream from qnrB (but not qnrA or qnrS) is a LexA binding site. qnrB was shown to be under SOS control by demonstrating that quinolone susceptibility decreased with increasing temperature in a strain with a recA441(Ts) allele, whereas qnrB expression increased in response to ciprofloxacin or mitomycin C in strains with an intact lexA gene.

引用

页码：821 / 823

页数：3

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