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Infection and Immunity, December 2005, p. 8039-8049, Vol. 73, No. 12
0019-9567/05/$08.00+0 doi:10.1128/IAI.73.12.8039-8049.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Mouse Intestine Selects Nonmotile flhDC Mutants of Escherichia coli MG1655 with Increased Colonizing Ability and Better Utilization of Carbon Sources
Mary P. Leatham,1
Sarah J. Stevenson,1
Eric J. Gauger,1
Karen A. Krogfelt,2
Jeremy J. Lins,1
Traci L. Haddock,1
Steven M. Autieri,1
Tyrrell Conway,3 and
Paul S. Cohen1*
Department of Cell and Molecular Biology, University of Rhode Island, Kingston, Rhode Island 02881,1
Department of Gastrointestinal Infections, Statens Seruminstitut, 2300 Copenhagen S, Denmark,2
Department of Botany and Microbiology, University of Oklahoma, Norman, Oklahoma 730193
Received 29 June 2005/
Returned for modification 24 August 2005/
Accepted 8 September 2005
D-Gluconate which is primarily catabolized via the Entner-Doudoroff (ED) pathway, has been implicated as being important for colonization of the streptomycin-treated mouse large intestine by Escherichia coli MG1655, a human commensal strain. In the present study, we report that an MG1655
edd mutant defective in the ED pathway grows poorly not only on gluconate as a sole carbon source but on a number of other sugars previously implicated as being important for colonization, including L-fucose, D-gluconate, D-glucuronate, N-acetyl-D-glucosamine, D-mannose, and D-ribose. Furthermore, we show that the mouse intestine selects mutants of MG1655
edd and wild-type MG1655 that have improved mouse intestine-colonizing ability and grow 15 to 30% faster on the aforementioned sugars. The mutants of MG1655
edd and wild-type MG1655 selected by the intestine are shown to be nonmotile and to have deletions in the flhDC operon, which encodes the master regulator of flagellar biosynthesis. Finally, we show that
flhDC mutants of wild-type MG1655 and MG1655
edd constructed in the laboratory act identically to those selected by the intestine; i.e., they grow better than their respective parents on sugars as sole carbon sources and are better colonizers of the mouse intestine.
* 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.
Editor: J. T. Barbieri
Infection and Immunity, December 2005, p. 8039-8049, Vol. 73, No. 12
0019-9567/05/$08.00+0 doi:10.1128/IAI.73.12.8039-8049.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
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Copyright © 2005 by the American Society for Microbiology. All rights reserved.