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Infect. Immun. doi:10.1128/IAI.00052-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

The Role of Motility and the flhDC Operon in Escherichia. coli MG1655 Colonization of the Mouse Intestine

Department of Cell and Molecular Biology, University of Rhode Island, Kingston, RI 02881; Department of Botany and Microbiology, University of Oklahoma, Norman, OK 73019

^* To whom correspondence should be addressed. Email: pco1697u{at}postoffice.uri.edu.

	Abstract

Previously, we reported that the mouse intestine selected mutants of E. coli MG1655 that have improved colonizing ability (Leatham et al, Infect. Immun. 73:8039-8049, 2005). These mutants grew 10-20% faster than their parent in mouse cecal mucus in vitro and 15-30% faster on several sugars found in the mouse intestine. The mutants were non-motile and had deletions of varying length beginning immediately downstream of an IS1 element located within the regulatory region of the flhDC operon, which encodes the master regulator of flagella biosynthesis, FlhD₄C₂. Here we show that during intestinal colonization by the wildtype E. coli MG1655, 45-50% became non-motile by day 3 post-feeding of the strain to mice and between 80 and 90% were non-motile by day 15 post-feeding. Ten non-motile mutants isolated from mice were sequenced and all were found to have flhDC deletions of varying lengths. Despite this strong selection, 10-20% of the E. coli MG1655 remained motile over a 15 day period, suggesting the existence of 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 FlhD₄C_2, 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