Mouse Intestine Selects Nonmotile
            <i>flhDC</i>
            Mutants of
            <i>Escherichia coli</i>
            MG1655 with Increased Colonizing Ability and Better Utilization of Carbon Sources

Leatham, Mary P.; Stevenson, Sarah J.; Gauger, Eric; Krogfelt, Karen A.; Lins, Jeremy J.; Haddock, Traci L.; Autieri, Steven M.; Conway, Tyrrell; Cohen, Paul S.

doi:10.1128/iai.73.12.8039-8049.2005

Cited by 89 publications

(148 citation statements)

References 47 publications

(52 reference statements)

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“…It was previously shown that a MG1655-derived strain with an flhD mutation that causes the strain to become nonmotile has a significant growth advantage in glycerol M9 minimal medium relative to the parent strain (20). Loss of motility in MG1655 adapted to growth in GMM has previously been observed (21).…”

Section: Resultsmentioning

confidence: 99%

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RNA polymerase mutants found through adaptive evolution reprogram Escherichia coli for optimal growth in minimal media

Conrad¹,

Frazier

Joyce

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

230

208

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Specific small deletions within the rpoC gene encoding the β′-subunit of RNA polymerase (RNAP) are found repeatedly after adaptation of Escherichia coli K-12 MG1655 to growth in minimal media. Here we present a multiscale analysis of these mutations. At the physiological level, the mutants grow 60% faster than the parent strain and convert the carbon source 15-35% more efficiently to biomass, but grow about 30% slower than the parent strain in rich medium. At the molecular level, the kinetic parameters of the mutated RNAP were found to be altered, resulting in a 4-to 30-fold decrease in open complex longevity at an rRNA promoter and a ∼10-fold decrease in transcriptional pausing, with consequent increase in transcript elongation rate. At a genome-scale, systems biology level, gene expression changes between the parent strain and adapted RNAP mutants reveal large-scale systematic transcriptional changes that influence specific cellular processes, including strong down-regulation of motility, acid resistance, fimbria, and curlin genes. RNAP genome-binding maps reveal redistribution of RNAP that may facilitate relief of a metabolic bottleneck to growth. These findings suggest that reprogramming the kinetic parameters of RNAP through specific mutations allows regulatory adaptation for optimal growth in new environments.kinetics | stringent response | transcription

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Section: Resultsmentioning

confidence: 99%

“…Cluster 2, representing strongly downregulated genes, was enriched for motility, chemotaxis, cell adhesion (fimbria and curli), and acid resistance genes. Down-regulation of these genes should provide a selective advantage in the growth environment, because their functions are costly in terms of energy but confer little or no benefit (20).…”

Section: Resultsmentioning

confidence: 99%

RNA polymerase mutants found through adaptive evolution reprogram Escherichia coli for optimal growth in minimal media

Conrad¹,

Frazier

Joyce

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

230

208

View full text Add to dashboard Cite

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“…Furthermore, selective pressures in the intestinal tract tend to counterselect the motility of E. coli. Hence, it was shown that mutations in the flhDC genes and in the two-component system envZ-ompR, drastically affecting the expression of the flagella, give a selective advantage in the intestine of mice (17,36). A parsimonious regulation of the expression of genes involved in motility is required probably because proteins constituting the flagella are immunogenic (4) and costly to produce (14).…”

Section: Discussionmentioning

confidence: 99%

Pathogenicity-Associated Islands in Extraintestinal PathogenicEscherichia coliAre Fitness Elements Involved in Intestinal Colonization

et al. 2010

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The virulence of many human pathogens does not seem to be an evolutionarily selected trait, but an accidental by-product of the selection that operates in another ecological context. We investigated the possibility that virulence of the extraintestinal pathogenic Escherichia coli (ExPEC) strains, which frequently cause disease in the host in which they asymptomatically colonize the intestine, is the consequence of commensalism. Most of the ExPEC virulence factors are clustered on genomic islands called pathogenicity-associated islands (PAIs). We constructed and characterized several mutants of the ExPEC 536 strain with either (i) deletions of each single PAI or (ii) a complete deletion of all seven PAIs. In vitro phenotypic characterization of 536 mutants showed that the seven PAIs were dispensable for growth in the absence of external stress, as well as under a range of biologically relevant stressors, i.e., serum, bile, and oxidative, nitrosative, hyperosmotic, and acidic stress. However, challenge against the wild-type (WT) strain in a murine model shows that the deletion of all seven PAIs drastically reduces the fitness of 536 during persistent intestinal colonization. This defect seems to be linked to the hypermotility observed for mutants devoid of all seven PAIs. In addition, we show that PAIs diminish fitness of their carrier during growth in urine, suggesting that urinary tract infections are unlikely to provide selective pressure for the maintenance of ExPEC PAIs. Our results are in accordance with the coincidental-evolution hypothesis postulating that extraintestinal E. coli virulence is a by-product of commensalism.

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“…To confirm this possibility, we used a strategy designed to provide the microbiota with a steady, high level of a rapidly metabolized carbon source. We previously showed that gluconate, which supports the growth of E. coli but is not absorbed by the host, is able to affect the outcome of experiments that depend on competition for gluconate (28). We reasoned that the constant availability of an excess supply of gluconate, provided by adding 2% gluconate to the drinking water of mice throughout the experiment, would rescue the dependence of colonized E. coli on stored glycogen.…”

Section: Vol 76 2008 In Vivo Maltose and Glycogen Metabolism 2535mentioning

confidence: 99%

Glycogen and Maltose Utilization by Escherichia coli O157:H7 in the Mouse Intestine

et al. 2008

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Mutant screens and transcriptome studies led us to consider whether the metabolism of glucose polymers, i.e., maltose, maltodextrin, and glycogen, is important for Escherichia coli colonization of the intestine. By using the streptomycin-treated mouse model, we found that catabolism of the disaccharide maltose provides a competitive advantage in vivo to pathogenic E. coli O157:H7 and commensal E. coli K-12, whereas degradation of exogenous forms of the more complex glucose polymer, maltodextrin, does not. The endogenous glucose polymer, glycogen, appears to play an important role in colonization, since mutants that are unable to synthesize or degrade glycogen have significant colonization defects. In support of the hypothesis that E. coli relies on internal carbon stores to maintain colonization during periods of famine, we found that by providing a constant supply of a readily metabolized sugar, i.e., gluconate, in the animal's drinking water, the competitive disadvantage of E. coli glycogen metabolism mutants is rescued. The results suggest that glycogen storage may be widespread in enteric bacteria because it is necessary for maintaining rapid growth in the intestine, where there is intense competition for resources and occasional famine. An important implication of this study is that the sugars used by E. coli are present in limited quantities in the intestine, making endogenous carbon stores valuable. Thus, there may be merit to combating enteric infections by using probiotics or prebiotics to manipulate the intestinal microbiota in such a way as to limit the availability of sugars preferred by E. coli O157:H7 and perhaps other pathogens.

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Mouse Intestine Selects Nonmotile flhDC Mutants of Escherichia coli MG1655 with Increased Colonizing Ability and Better Utilization of Carbon Sources

Cited by 89 publications

References 47 publications

RNA polymerase mutants found through adaptive evolution reprogram Escherichia coli for optimal growth in minimal media

RNA polymerase mutants found through adaptive evolution reprogram Escherichia coli for optimal growth in minimal media

Pathogenicity-Associated Islands in Extraintestinal PathogenicEscherichia coliAre Fitness Elements Involved in Intestinal Colonization

Glycogen and Maltose Utilization by Escherichia coli O157:H7 in the Mouse Intestine

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