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Journal of Bacteriology, March 2008, p. 1879-1890, Vol. 190, No. 6
0021-9193/08/$08.00+0     doi:10.1128/JB.01796-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

CmeR Functions as a Pleiotropic Regulator and Is Required for Optimal Colonization of Campylobacter jejuni In Vivo{triangledown}

Baoqing Guo,1,{dagger} Ying Wang,1,{dagger},{ddagger} Feng Shi,1 Yi-Wen Barton,1 Paul Plummer,1 Donald L. Reynolds,1 Dan Nettleton,2 Tara Grinnage-Pulley,1 Jun Lin,1,§ and Qijing Zhang1*

Departments of Veterinary Microbiology and Preventive Medicine,1 Statistics, Iowa State University, Ames, Iowa 500112

Received 13 November 2007/ Accepted 21 December 2007

CmeR functions as a transcriptional repressor modulating the expression of the multidrug efflux pump CmeABC in Campylobacter jejuni. To determine if CmeR also regulates other genes in C. jejuni, we compared the transcriptome of the cmeR mutant with that of the wild-type strain using a DNA microarray. This comparison identified 28 genes that showed a ≥2-fold change in expression in the cmeR mutant. Independent real-time quantitative reverse transcription-PCR experiments confirmed 27 of the 28 differentially expressed genes. The CmeR-regulated genes encode membrane transporters, proteins involved in C4-dicarboxylate transport and utilization, enzymes for biosynthesis of capsular polysaccharide, and hypothetical proteins with unknown functions. Among the genes whose expression was upregulated in the cmeR mutant, Cj0561c (encoding a putative periplasmic protein) showed the greatest increase in expression. Subsequent experiments demonstrated that this gene is strongly repressed by CmeR. The presence of the known CmeR-binding site, an inverted repeat of TGTAAT, in the promoter region of Cj0561c suggests that CmeR directly inhibits the transcription of Cj0561c. Similar to expression of cmeABC, transcription of Cj0561c is strongly induced by bile compounds, which are normally present in the intestinal tracts of animals. Inactivation of Cj0561c did not affect the susceptibility of C. jejuni to antimicrobial compounds in vitro but reduced the fitness of C. jejuni in chickens. Loss-of-function mutation of cmeR severely reduced the ability of C. jejuni to colonize chickens. Together, these findings indicate that CmeR governs the expression of multiple genes with diverse functions and is required for Campylobacter adaptation in the chicken host.

* Corresponding author. Mailing address: Department of Veterinary Microbiology and Preventive Medicine, 1116 Veterinary Medicine Complex, Iowa State University, Ames, IA 50011. Phone: (515) 294-2038. Fax: (515) 294-8500. E-mail: zhang123{at}iastate.edu

{triangledown} Published ahead of print on 4 January 2008.

{dagger} B.G. and Y.W. contributed equally to this work.

{ddagger} Present address: Department of Biochemistry, Cellular and Molecular Biology, The University of Tennessee, Knoxville, TN 37996.

§ Present address: Department of Animal Science, University of Tennessee, Knoxville, TN 37996.

Journal of Bacteriology, March 2008, p. 1879-1890, Vol. 190, No. 6
0021-9193/08/$08.00+0     doi:10.1128/JB.01796-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Wang, L., Jeon, B., Sahin, O., Zhang, Q. (2009). Identification of an Arsenic Resistance and Arsenic-Sensing System in Campylobacter jejuni. Appl. Environ. Microbiol. 75: 5064-5073 [Abstract] [Full Text]  


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