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Journal of Bacteriology, August 2006, p. 5851-5858, Vol. 188, No. 16
0021-9193/06/$08.00+0     doi:10.1128/JB.00301-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

N-Acetyl-D-Glucosamine Induces the Expression of Multidrug Exporter Genes, mdtEF, via Catabolite Activation in Escherichia coli

Hidetada Hirakawa,^1,2,3, Yoshihiko Inazumi,^1,2,3 Yasuko Senda,^1,2,3 Asuka Kobayashi,^1,2,3 Takahiro Hirata,^1,2,3 Kunihiko Nishino,^1,2,3 and Akihito Yamaguchi^1,2,3*

Department of Cell Membrane Biology, Institute of Scientific and Industrial Research, Osaka University, Ibaraki, Osaka 567-0047, Japan,¹ Graduate School of Pharmaceutical Sciences, Osaka University, Suita, Osaka 565-0871, Japan,² CREST, Japan Science and Technology Corporation, Osaka 567-0047, Japan³

Received 1 March 2006/ Accepted 25 May 2006

The expression of MdtEF, a multidrug exporter in Escherichia coli, is positively controlled through multiple signaling pathways, but little is known about signals that induce MdtEF expression. In this study, we investigated compounds that induce the expression of the mdtEF genes and found that out of 20 drug exporter genes in E. coli, the expression of mdtEF is greatly induced by N-acetyl-D-glucosamine (GlcNAc). The induction of mdtEF by GlcNAc is not mediated by the evgSA, ydeO, gadX, and rpoS signaling pathways that have been known to regulate mdtEF expression. On the other hand, deletion of the nagE gene, encoding the phosphotransferase (PTS) system for GlcNAc, prevented induction by GlcNAc. The induction of mdtEF by GlcNAc was also greatly inhibited by the addition of cyclic AMP (cAMP) and completely abolished upon deletion of the cAMP receptor protein gene (crp). Other PTS sugars, glucose and D-glucosamine, also induced mdtEF gene expression. These results suggest that mdtEF expression is stimulated through catabolite control.

Supplemental material for this article may be found at http://jb.asm.org/.

Present address: Department of Microbiology and Molecular Genetics, Graduate School of Pharmaceutical Sciences, Chiba University, Chiba, 263-8522, Japan.

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