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Infection and Immunity, July 2007, p. 3315-3324, Vol. 75, No. 7
0019-9567/07/$08.00+0     doi:10.1128/IAI.00052-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Role of Motility and the flhDC Operon in Escherichia coli MG1655 Colonization of the Mouse Intestine{triangledown}

Eric J. Gauger,1,{dagger} Mary P. Leatham,1 Regino Mercado-Lubo,1 David C. Laux,1 Tyrrell Conway,2 and Paul S. Cohen1*

Department of Cell and Molecular Biology, University of Rhode Island, Kingston, Rhode Island 02881,1 Department of Botany and Microbiology, University of Oklahoma, Norman, Oklahoma 730192

Received 10 January 2007/ Returned for modification 4 March 2007/ Accepted 10 April 2007

Previously, we reported that the mouse intestine selected mutants of Escherichia coli MG1655 that have improved colonizing ability (M. P. Leatham et al., Infect. Immun. 73:8039-8049, 2005). These mutants grew 10 to 20% faster than their parent in mouse cecal mucus in vitro and 15 to 30% faster on several sugars found in the mouse intestine. The mutants were nonmotile and had deletions of various lengths beginning immediately downstream of an IS1 element located within the regulatory region of the flhDC operon, which encodes the master regulator of flagellum biosynthesis, FlhD4C2. Here we show that during intestinal colonization by wild-type E. coli strain MG1655, 45 to 50% of the cells became nonmotile by day 3 after feeding of the strain to mice and between 80 and 90% of the cells were nonmotile by day 15 after feeding. Ten nonmotile mutants isolated from mice were sequenced, and all were found to have flhDC deletions of various lengths. Despite this strong selection, 10 to 20% of the E. coli MG1655 cells remained motile over a 15-day period, suggesting that there is an as-yet-undefined intestinal niche in which motility is an advantage. The deletions appear to be selected in the intestine for two reasons. First, genes unrelated to motility that are normally either directly or indirectly repressed by FlhD4C2 but can contribute to maximum colonizing ability are released from repression. Second, energy normally used to synthesize flagella and turn the flagellar motor is redirected to growth.


* Corresponding author. Mailing address: Department of Cell and Molecular Biology, University of Rhode Island, Kingston, RI 02881. Phone: (401) 874-5920. Fax: (401) 874-2202. E-mail: pco1697u{at}postoffice.uri.edu

{triangledown} Published ahead of print on 16 April 2007.

Editor: J. B. Bliska

{dagger} Present address: Intervet Inc., P.O. Box 318, Millsboro, DE 19966.


Infection and Immunity, July 2007, p. 3315-3324, Vol. 75, No. 7
0019-9567/07/$08.00+0     doi:10.1128/IAI.00052-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.







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