抑制因子lexA
SOS响应
生物
微生物学
金黄色葡萄球菌
严格的回应
减压
西格玛因子
调节器
多药耐受
铜绿假单胞菌
环丙沙星
大肠杆菌
遗传学
抗生素
抑制因子
转录因子
基因
细菌
RNA聚合酶
生物膜
基因表达
心理压抑
作者
Ryan T. Cirz,Marcus B. Jones,Neill A. Gingles,Timothy D. Minogue,Behnam Jarrahi,Scott N. Peterson,Floyd E. Romesberg
摘要
ABSTRACT Staphylococcus aureus infections can be difficult to treat due to both multidrug resistance and the organism's remarkable ability to persist in the host. Persistence and the evolution of resistance may be related to several complex regulatory networks, such as the SOS response, which modifies transcription in response to environmental stress. To understand how S. aureus persists during antibiotic therapy and eventually emerges resistant, we characterized its global transcriptional response to ciprofloxacin. We found that ciprofloxacin induces prophage mobilization as well as significant alterations in metabolism, most notably the up-regulation of the tricarboxylic acid cycle. In addition, we found that ciprofloxacin induces the SOS response, which we show, by comparison of a wild-type strain and a non-SOS-inducible lexA mutant strain, includes the derepression of 16 genes. While the SOS response of S. aureus is much more limited than those of Escherichia coli and Bacillus subtilis , it is similar to that of Pseudomonas aeruginosa and includes RecA, LexA, several hypothetical proteins, and a likely error-prone Y family polymerase whose homologs in other bacteria are required for induced mutation. We also examined induced mutation and found that either the inability to derepress the SOS response or the lack of the LexA-regulated polymerase renders S. aureus unable to evolve antibiotic resistance in vitro in response to UV damage. The data suggest that up-regulation of the tricarboxylic acid cycle and induced mutation facilitate S. aureus persistence and evolution of resistance during antibiotic therapy.
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