Identification and characterization of the AcrR/AcrAB system of a pathogenic Edwardsiella tarda strain | |
Hou, Jin-hui1,2,3; Hu, Yong-hua1,2,3; Zhang, Min1,2,3; Sun, Li1 | |
刊名 | JOURNAL OF GENERAL AND APPLIED MICROBIOLOGY
![]() |
2009-06-01 | |
卷号 | 55期号:3页码:191-199 |
关键词 | Acrab Acriflavine Acrr Antimicrobial Resistance Methyl Viologen Virulence |
ISSN号 | 0022-1260 |
文献子类 | Article |
英文摘要 | 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.; 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. |
学科主题 | Biotechnology & Applied Microbiology ; Microbiology |
语种 | 英语 |
WOS记录号 | WOS:000268828300003 |
公开日期 | 2010-12-22 |
内容类型 | 期刊论文 |
源URL | [http://ir.qdio.ac.cn/handle/337002/2917] ![]() |
专题 | 海洋研究所_实验海洋生物学重点实验室 |
作者单位 | 1.Chinese Acad Sci, Inst Oceanol, Qingdao 266071, Peoples R China 2.Chinese Acad Sci, Grad Univ, Beijing, Peoples R China 3.Xuzhou Inst Technol, Xuzhou, Peoples R China |
推荐引用方式 GB/T 7714 | Hou, Jin-hui,Hu, Yong-hua,Zhang, Min,et al. Identification and characterization of the AcrR/AcrAB system of a pathogenic Edwardsiella tarda strain[J]. JOURNAL OF GENERAL AND APPLIED MICROBIOLOGY,2009,55(3):191-199. |
APA | Hou, Jin-hui,Hu, Yong-hua,Zhang, Min,&Sun, Li.(2009).Identification and characterization of the AcrR/AcrAB system of a pathogenic Edwardsiella tarda strain.JOURNAL OF GENERAL AND APPLIED MICROBIOLOGY,55(3),191-199. |
MLA | Hou, Jin-hui,et al."Identification and characterization of the AcrR/AcrAB system of a pathogenic Edwardsiella tarda strain".JOURNAL OF GENERAL AND APPLIED MICROBIOLOGY 55.3(2009):191-199. |
个性服务 |
查看访问统计 |
相关权益政策 |
暂无数据 |
收藏/分享 |
除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。
修改评论