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J Antimicrob Chemother. 2010 Jun;65(6):1171-7. doi: 10.1093/jac/dkq114. Epub 2010 Apr 21.

Signature gene expression profile of triclosan-resistant Escherichia coli.

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1
Systems Microbiology Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 305-806, Korea.

Abstract

OBJECTIVES:

To gain further insight into the defence mechanisms against triclosan in a mutant derived from an Escherichia coli strain carrying the triclosan-resistant target enzyme, FabI(G93V).

METHODS:

An E. coli imp4231 FabI(G93V) strain was constructed by replacing intact fabI with a linear DNA cassette, fabI(G93V)-CmR, that contains a single mutation, GGT to GTT, at codon 93 of fabI(G93V) and a chloramphenicol resistance gene (CmR) as a marker for the mutant allele by a Red-mediated recombination system. Using this E. coli imp4231 FabI(G93V) strain, nitrosoguanidine (NTG) mutagenesis was performed to generate E. coli IFNs [imp4231 FabI(G93V) treated with NTG] displaying higher MICs of triclosan than its parent strain. The genes overexpressed in E. coli IFN4 were identified by DNA microarray analysis.

RESULTS:

An E. coli imp4231 FabI(G93V) strain displays approximately 400-fold increased MICs of triclosan (MIC approximately 8 mg/L) compared with the parent strain (MIC approximately 0.02 mg/L). Furthermore, E. coli IFN4 has the highest MIC of triclosan (MIC approximately 80 mg/L). DNA microarray analysis of E. coli IFN4 shows that many genes involved in the biosynthesis of membrane proteins, including transporters, reductases/dehydrogenases and stress response regulators, were highly expressed in the mutant.

CONCLUSIONS:

These results strongly indicate that E. coli IFN cells might protect themselves from triclosan by activating various defence mechanisms, such as (i) changing efflux activities; (ii) capturing the triclosan; and (iii) increasing the expression of important regulators or metabolic enzymes.

PMID:
20410062
DOI:
10.1093/jac/dkq114
[Indexed for MEDLINE]
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