Identification and characterization of the AcrR/AcrAB system of a pathogenic Edwardsiella tarda strain
Identification and characterization of the AcrR/AcrAB system of a pathogenic Edwardsiella tarda strain
复制标题
迟缓爱德华氏菌致病菌株 AcrR/AcrAB 系统的鉴定和表征
DOI：
10.2323/jgam.55.191
复制
发表时间：
2009-06-01
影响因子：
1.2
通讯作者：
Sun, Li
中科院分区：
文献类型：
--
作者：
Hou, Jin-hui;Hu, Yong-hua;Sun, Li
迟缓爱德华氏菌是主要的海洋病原体之一，可以感染多种养殖海洋物种。在这项研究中，acrR-acrAB 簇是从 TX1 中克隆出来的，TX1 是一种从病鱼中分离出来的致病性 E. tarda 菌株。 AcrR 和 AcrAB 被发现参与对吖啶黄和甲基紫精的耐药性，从而正向调节 acrAB 的表达。 AcrR 负向调节其自身表达和 acrAB 操纵子的表达，最有可能是通过与与 acrA (PacrA) 推定启动子重叠的 24 bp 操纵子位点相互作用。 AcrR 对 PacrA 的抑制作用可以通过吖啶黄、甲基紫精和溴化乙锭缓解，它们的存在都会增强 PacrA 的转录。通过将过表达 acrR 的质粒引入 TX1 来中断 acrR 的调节表达，会影响应激条件下的生长、AI-2 的产生和细菌毒力。此外，突变分析还发现了一种组成型活性 AcrR 突变体（称为 N215），该突变体表现出完全的阻遏活性，但与诱导剂相互作用的能力受损。与野生型 acrR 的过表达相比，N215 的过表达对 TX1 产生相同但稍强的影响。
Edwardsielia tarda is one of the leading marine pathogens that can infect a wide range of cultured marine species. In this study, the acrR-acrAB cluster was cloned from TX1, a pathogenic E. tarda strain isolated from diseased fish. AcrR and AcrAB were found to be involved in resistance against acriflavine and methyl viologen, which positively regulate the expression of acrAB. AcrR negatively regulates its own expression and the expression of the acrAB operon, most likely by interacting with a 24-bp operator site that overlaps the putative promoter of acrA (PacrA). The repressive effect of AcrR on PacrA could be relieved by acriflavine, methyl viologen, and ethidium bromide, the presence of each of which enhanced transcription from PacrA. Interruption of the regulated expression of acrR by introducing into TX1 a plasmid that overexpresses acrR affected growth under stress conditions, AI-2 production, and bacterial virulence. In addition, mutational analyses identified a constitutively active AcrR mutant (named N215), which exhibits full repressor activity but is impaired in its ability to interact with the inducer. Overexpression of N215 produced the same kind of but moderately stronger effect on TX1 compared to that produced by overexpression of the wild-type acrR.