title: The streptomycin-treated mouse intestine selects Escherichia coli envZ missense mutants that interact with dense and diverse intestinal microbiota.
abstract: Previously, we reported that the streptomycin-treated mouse intestine selected nonmotile Escherichia coli MG1655 flhDC deletion mutants of E. coli MG1655 with improved colonizing ability that grow 15% faster in vitro in 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 motile E. coli MG1655 are envZ missense mutants that are also better colonizers of the mouse intestine than E. coli MG1655. One of the flhDC mutants, E. coli MG1655 ΔflhD, and one of the envZ missense mutants, E. coli MG1655 mot-1, were studied further. E. coli MG1655 mot-1 is more resistant to bile salts and colicin V than E. coli MG1655 ΔflhD and grows ca. 15% slower in vitro in mouse cecal mucus and on several sugars present in mucus compared to E. coli MG1655 ΔflhD but grows 30% faster on galactose. Moreover, E. coli MG1655 mot-1 and E. coli MG1655 ΔflhD appear to colonize equally well in one intestinal niche, but E. coli MG1655 mot-1 appears to use galactose to colonize a second, smaller intestinal niche either not colonized or colonized poorly by E. coli MG1655 ΔflhD. Evidence is also presented that E. coli MG1655 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.
authors.affiliation: Department of Cell and Molecular Biology, University of Rhode Island, Kingston, Rhode Island, USA.
authors.forename: Mary P
authors.initials: MP
authors.lastname: Leatham-Jensen
authors.forename: Jakob
authors.initials: J
authors.lastname: Frimodt-Møller
authors.forename: Jimmy
authors.initials: J
authors.lastname: Adediran
authors.forename: Matthew E
authors.initials: ME
authors.lastname: Mokszycki
authors.forename: Megan E
authors.initials: ME
authors.lastname: Banner
authors.forename: Joyce E
authors.initials: JE
authors.lastname: Caughron
authors.forename: Karen A
authors.initials: KA
authors.lastname: Krogfelt
authors.forename: Tyrrell
authors.initials: T
authors.lastname: Conway
authors.forename: Paul S
authors.initials: PS
authors.lastname: Cohen
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D001425:Bacterial Outer Membrane Proteins / Q000235:genetics / Q000378:metabolism*; D018441:Biofilms; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D029968:Escherichia coli Proteins / Q000235:genetics / Q000378:metabolism*; D015964:Gene Expression Regulation, Bacterial; D007422:Intestines / Q000382:microbiology*; D051379:Mice; D009097:Multienzyme Complexes / Q000235:genetics / Q000378:metabolism*; D020125:Mutation, Missense; D012641:Selection, Genetic; D013307:Streptomycin / Q000494:pharmacology*
chemical_list: D001425:Bacterial Outer Membrane Proteins; D029968:Escherichia coli Proteins; D009097:Multienzyme Complexes; C057843:envZ protein, E coli; D013307:Streptomycin