GENES ACRA AND ACRB ENCODE A STRESS-INDUCED EFFLUX SYSTEM OF ESCHERICHIA-COLI
GENES ACRA AND ACRB ENCODE A STRESS-INDUCED EFFLUX SYSTEM OF ESCHERICHIA-COLI
复制标题
DOI：
10.1111/j.1365-2958.1995.tb02390.x
复制
发表时间：
1995-04-01
影响因子：
3.6
通讯作者：
HEARST, JE
中科院分区：
文献类型：
--
作者：
MA, D;COOK, DN;HEARST, JE
acrA或acrS（以前称为acrE）基因的定义突变增加了大肠杆菌对一系列小抑制剂分子的敏感性。acrAB的缺失增加了对头孢噻吩和头孢噻啶的敏感性，但这些β-内酰胺类药物穿过外膜的渗透性并未增加。这一发现是不一致的早期假设，acrAB突变增加药物敏感性，通过增加外膜的渗透性，并支持我们的模型，acrAB编码的多药外排泵。肠道细菌如E.大肠杆菌富含胆汁盐和脂肪酸。发现acrAB缺失突变体对胆盐和癸酸盐过敏。此外，acrAB表达通过在5 mM癸酸中生长而升高。这些结果表明AcrAB的一个主要生理功能是保护E.大肠杆菌对这些和其他疏水性抑制剂。acrAB的转录通过其他胁迫条件增加，包括4%乙醇、0.5M NaCl和Luria-Bertani培养基中的固定相。最后，acrAB表达在mar（多重抗生素抗性）突变体中显示增加。
Defined mutations of acrA or acrS (formerly acrE) genes increased the susceptibility of Escherichia coli to a range of small inhibitor molecules. Deletion of acrAB increased susceptibility to cephalothin and cephaloridine, but the permeability of these beta-lactams across the outer membrane was not increased. This finding is inconsistent with the earlier hypothesis that acrAB mutations increase drug susceptibility by increasing the permeability of the outer membrane, and supports our model that acrAB codes for a multi-drug efflux pump. The natural environment of an enteric bacterium such as E. coli is enriched in bile salts and fatty acids. An acrAB deletion mutant was found to be hypersusceptible to bile salts and to decanoate. In addition, acrAB expression was elevated by growth in 5mM decanoate. These results suggest that one major physiological function of AcrAB is to protect E. coli against these and other hydrophobic inhibitors. Transcription of acrAB is increased by other stress conditions including 4% ethanol, 0.5M NaCl, and stationary phase in Luria-Bertani medium. Finally, acrAB expression was shown to be increased in mar (multiple-antibiotic-resistant) mutants.