RESISTANCE OF NEISSERIA-GONORRHOEAE TO ANTIMICROBIAL HYDROPHOBIC AGENTS IS MODULATED BY THE MTRRCDE EFFLUX SYSTEM

Citation
Ke. Hagman et al., RESISTANCE OF NEISSERIA-GONORRHOEAE TO ANTIMICROBIAL HYDROPHOBIC AGENTS IS MODULATED BY THE MTRRCDE EFFLUX SYSTEM, Microbiology, 141, 1995, pp. 611-622
Citations number
43
Categorie Soggetti
Microbiology
Journal title
ISSN journal
13500872
Volume
141
Year of publication
1995
Part
3
Pages
611 - 622
Database
ISI
SICI code
1350-0872(1995)141:<611:RONTAH>2.0.ZU;2-8
Abstract
The mtr (multiple transferable resistance) system of Neisseria gonorrh oeae determines levels of gonococcal resistance to hydrophobic agents (HAs), including detergent-like fatty acids and bile salts that bathe certain mucosal surfaces. The genetic organization of the mtr system w as determined and found to consist of the mtrR gene, which encodes a t ranscriptional regulator (MtrR), and three tandemly linked genes terme d mtrCDE. The mtrCDE genes were organized in the same apparent transcr iptional unit, upstream and divergent from the mtrR gene. The mtrCDE-e ncoded proteins of N. gonorrhoeae were analogous to a family of bacter ial efflux/transport proteins, notable the MexABOprK proteins of Pseud omonas aeruginosa and the AcrAE and EnvCD proteins of Escherichia coli , that mediate resistance to drugs, dyes, and detergents. Inactivation of the mtrC gene resulted in loss of the MtrC lipoprotein and rendere d gonococci hypersusceptible to structurally diverse HAs; this reveale d the importance of the mtr system in determining HA(R) in gonococci. Further support for a role of the mtrCDE gene complex in determining l evels of HA(R) in gonococci was evident when transformants bearing mut ations in the mtrR gene were analysed. In this respect, missense and a nd null mutations in the mtrR gene were found to result in increased l evels of MtrC and HA(R). However, high levels of MtrC and HA(R), simil ar to those observed for clinical isolates, were associated with a sin gle bp deletion in a 13 bp inverted repeat sequence that intervened th at divergent mtrR and mtrC genes. We propose that the 13 bp inverted-r epeat sequence represents a transcriptional control element that regul ates expression of the mtrRCDE gene complex, thereby modulating levels of gonococcal susceptibility to HAs.