Format

Send to

Choose Destination
FEMS Microbiol Lett. 2015 Jan;362(1):1-8. doi: 10.1093/femsle/fnu013. Epub 2014 Dec 4.

Role of transcription factor NimR (YeaM) in sensitivity control of Escherichia coli to 2-nitroimidazole.

Author information

1
Research Center for Human and Environmental Sciences, Shinshu University, Ueda, Nagano 386-8567, Japan.
2
Department of Frontier Bioscience, Hosei University, Koganei, Tokyo 184-8584, Japan.
3
Department of Frontier Bioscience, Hosei University, Koganei, Tokyo 184-8584, Japan Research Center for Micro-Nano Technology, Hosei University, Koganei, Tokyo 184-8584, Japan aishiham@hosei.ac.jp.

Abstract

The binding site(s) on the Escherichia coli genome was determined for an uncharacterized AraC/XylS superfamily transcription factor YeaM by using the in vitro genomic SELEX screening system. The only one clear binding target of YeaM was found to locate in the spacer between the divergently transcribed yeaM and yeaN genes. After the phenotype microarray analysis, the major facilitator superfamily transporter YeaN was found to confer E. coli the resistance to 2-nitroimidazole, the antibacterial and antifungal antibiotic, suggesting that YeaN plays a role in 2-nitromidazole efflux. Purified YeaM bound to three sites within this yeaM-yeaN spacer region. Several lines of in vitro and in vivo evidence indicate that YeaM regulates transcription of both the yeaM gene itself and the yeaNO operon. Taken together we propose to rename yeaN to nimT (nitroimidazole transporter) and yeaM to nimR (regulator of nimT).

KEYWORDS:

2-nitroimidazole; Escherichia coli; efflux pump NimT; genomic SELEX; transcription factor NimR

PMID:
25790494
DOI:
10.1093/femsle/fnu013
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Silverchair Information Systems Icon for Wiley
Loading ...
Support Center