The Streptomycin-Treated Mouse Intestine SelectsEscherichia coli envZMissense Mutants That Interact with Dense and Diverse Intestinal Microbiota

Abstract

ABSTRACTPreviously, we reported that the streptomycin-treated mouse intestine selected nonmotileEscherichia coliMG1655flhDCdeletion mutants ofE. coliMG1655 with improved colonizing ability that grow 15% fasterin vitroin mouse cecal mucus and 15 to 30% faster on sugars present in mucus (M. P. Leatham et al., Infect. Immun. 73:8039–8049, 2005). Here, we report that the 10 to 20% remaining motileE. coliMG1655 areenvZmissense mutants that are also better colonizers of the mouse intestine thanE. coliMG1655. One of theflhDCmutants,E. coliMG1655 ΔflhD, and one of theenvZmissense mutants,E. coliMG1655 mot-1, were studied further.E. coliMG1655 mot-1 is more resistant to bile salts and colicin V thanE. coliMG1655 ΔflhDand grows ca. 15% slowerin vitroin mouse cecal mucus and on several sugars present in mucus compared toE. coliMG1655 ΔflhDbut grows 30% faster on galactose. Moreover,E. coliMG1655 mot-1 andE. coliMG1655 ΔflhDappear to colonize equally well in one intestinal niche, butE. coliMG1655 mot-1 appears to use galactose to colonize a second, smaller intestinal niche either not colonized or colonized poorly byE. coliMG1655 ΔflhD. Evidence is also presented thatE. coliMG1655 is a minority member of mixed bacterial biofilms in the mucus layer of the streptomycin-treated mouse intestine. We offer a hypothesis, which we call the “Restaurant” hypothesis, that explains how nutrient acquisition in different biofilms comprised of different anaerobes can account for our results.