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fucAO and E. coli Nissle 1917
fucAO Mutants in the Mouse Intestine and in M9 Minimal Medium
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 15 June 2007/ Returned for modification 30 July 2007/ Accepted 7 August 2007
Escherichia coli MG1655 uses several sugars for growth in the mouse intestine. To determine the roles of L-fucose and D-ribose, an E. coli MG1655
fucAO mutant and an E. coli MG1655
rbsK mutant were fed separately to mice along with wild-type E. coli MG1655. The E. coli MG1655
fucAO mutant colonized the intestine at a level 2 orders of magnitude lower than that of the wild type, but the E. coli MG1655
rbsK mutant and the wild type colonized at nearly identical levels. Surprisingly, an E. coli MG1655
fucAO
rbsK mutant was eliminated from the intestine by either wild-type E. coli MG1655 or E. coli MG1655
fucAO, suggesting that the
fucAO mutant switches to ribose in vivo. Indeed, in vitro growth experiments showed that L-fucose stimulated utilization of D-ribose by the E. coli MG1655
fucAO mutant but not by an E. coli MG1655
fucK mutant. Since the
fucK mutant cannot convert L-fuculose to L-fuculose-1-phosphate, whereas the
fucAO mutant accumulates L-fuculose-1-phosphate, the data suggest that L-fuculose-1-phosphate stimulates growth on ribose both in the intestine and in vitro. An E. coli Nissle 1917
fucAO mutant, derived from a human probiotic commensal strain, acted in a manner identical to that of E. coli MG1655
fucAO in vivo and in vitro. Furthermore, L-fucose at a concentration too low to support growth stimulated the utilization of ribose by the wild-type E. coli strains in vitro. Collectively, the data suggest that L-fuculose-1-phosphate plays a role in the regulation of ribose usage as a carbon source by E. coli MG1655 and E. coli Nissle 1917 in the mouse intestine.
Published ahead of print on 20 August 2007.
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