Related Experiment Video
Updated: Jun 13, 2026
Population and Single-Cell Analysis of Antibiotic Persistence in Escherichia coli
Published on: March 24, 2023
Signature gene expression profile of triclosan-resistant Escherichia coli
Byung Jo Yu1, Jung Ae Kim, Jae-Gu Pan
1Systems Microbiology Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 305-806, Korea.
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.
