Draft Genome Sequence of Escherichia coli Strain Nissle 1917 (Serovar O6:K5:H1)

Cress, Brady F.; Linhardt, Robert J.; Koffas, Mattheos

doi:10.1128/genomea.00047-13

Cited by 31 publications

(28 citation statements)

References 8 publications

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“…In spite of EcN's long-term use in medicine, its comprehensive investigations by many research groups, and its proven clinical efficacy, the genomic DNA sequence of this probiotic bacterium has only been published as a draft (Cress et al, 2013). Here we report EcN's complete and annotated genome sequence.…”

mentioning

confidence: 91%

Complete genome sequence of the Gram-negative probiotic Escherichia coli strain Nissle 1917

Reister

Hoffmeier

Krezdorn

et al. 2014

Journal of Biotechnology

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mentioning

confidence: 91%

Complete genome sequence of the Gram-negative probiotic Escherichia coli strain Nissle 1917

Reister

Hoffmeier

Krezdorn

et al. 2014

Journal of Biotechnology

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“…We initially attempted to colonize mice with two human commensal E. coli strains, Nissle 1917 and HS (4,(27)(28)(29), without continuous selection with an antibiotic. However, in both cases, we found that colonization was often relatively short-lived and showed significant mouse-tomouse variability (data not shown).…”

Section: Isolation and Characterization Of Mp1mentioning

confidence: 99%

Escherichia coli Isolate for Studying Colonization of the Mouse Intestine and Its Application to Two-Component Signaling Knockouts

et al. 2014

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The biology of Escherichia coli in its primary niche, the animal intestinal tract, is remarkably unexplored. Studies with the streptomycin-treated mouse model have produced important insights into the metabolic requirements for Escherichia coli to colonize mice. However, we still know relatively little about the physiology of this bacterium growing in the complex environment of an intestine that is permissive for the growth of competing flora. We have developed a system for studying colonization using an E. coli strain, MP1, isolated from a mouse. MP1 is genetically tractable and does not require continuous antibiotic treatment for stable colonization. As an application of this system, we separately knocked out each two-component system response regulator in MP1 and performed competitions against the wild-type strain. We found that only three response regulators, ArcA, CpxR, and RcsB, produce strong colonization defects, suggesting that in addition to anaerobiosis, adaptation to cell envelope stress is a critical requirement for E. coli colonization of the mouse intestine. We also show that the response regulator OmpR, which had previously been hypothesized to be important for adaptation between in vivo and ex vivo environments, is not required for MP1 colonization due to the presence of a third major porin. Escherichia coli is one of the most extensively studied and bestcharacterized organisms. Its high growth rate, facile genetics, and simple nutritional requirements have made this bacterium an excellent model system for studying basic aspects of molecular biology and bacteriology and the primary host for DNA and protein engineering. The physiology of E. coli growth and survival under diverse conditions has been intensively studied, and a significant fraction of E. coli gene products and regulatory networks have been characterized. However, for such a well-studied organism, we know remarkably little about the biology of E. coli in its primary niche: the animal gastrointestinal tract.E. coli is generally the most abundant aerobe in the intestines of warm-blooded vertebrates, although its numbers vary considerably with animal host and geography (1-3). As a species, this bacterium has a remarkable genetic diversity; the number of genes in common among fully sequenced isolates is less than half the number of genes in any individual strain (4-6). Some E. coli strains are pathogenic, depending on the host and site of infection (3, 7-9), and have been intensively studied to understand the factors controlling their virulence. However, the majority of E. coli strains associated with animals are believed to be part of the normal flora of the intestine, growing asymptomatically as commensals.Most of our knowledge about E. coli colonization of the animal intestine comes from studies with streptomycin-resistant strains colonizing mice fed streptomycin continuously in their drinking water (10, 11). This streptomycin-treated mouse model has played a key role in the characterization of the growth of E. coli in the intestine a...

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“…In vitro chemoenzymatic synthesis of bioengineered heparin and oligosaccharides has shown promise as an alternative approach to producing the anticoagulant drug from nonanimal sources (3)(4)(5). As the starting material for the cost-effective synthesis of novel anticoagulant drugs, the availability of heparosan is a significant concern (6)(7)(8). Recent studies show that carbon sources have differential impacts on the yield of heparosan (26,27).…”

Section: Discussionmentioning

confidence: 99%

“…As the starting carbon backbone for the cost-effective synthesis of bioengineered heparin, the availability of heparosan is a big concern (6)(7)(8)(9). Heparosan is extracted from the capsular polysaccharide (CPS) of Escherichia coli K5, Pasteurella multocida, and E. coli strain Nissle 1917 (EcN) (8,10,11).…”

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confidence: 99%

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Cyclic AMP (cAMP) Receptor Protein-cAMP Complex Regulates Heparosan Production in Escherichia coli Strain Nissle 1917

Yan

Bao

Zhao

et al. 2015

Appl Environ Microbiol

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cHeparosan serves as the starting carbon backbone for the chemoenzymatic synthesis of heparin, a widely used clinical anticoagulant drug. The availability of heparosan is a significant concern for the cost-effective synthesis of bioengineered heparin. The carbon source is known as the pivotal factor affecting heparosan production. However, the mechanism by which carbon sources control the biosynthesis of heparosan is unclear. In this study, we found that the biosynthesis of heparosan was influenced by different carbon sources. Glucose inhibits the biosynthesis of heparosan, while the addition of either fructose or mannose increases the yield of heparosan. Further study demonstrated that the cyclic AMP (cAMP)-cAMP receptor protein (CRP) complex binds to the upstream region of the region 3 promoter and stimulates the transcription of the gene cluster for heparosan biosynthesis. Site-directed mutagenesis of the CRP binding site abolished its capability of binding CRP and eliminated the stimulative effect on transcription.1 H nuclear magnetic resonance (NMR) analysis was further performed to determine the Escherichia coli strain Nissle 1917 (EcN) heparosan structure and quantify extracellular heparosan production. Our results add to the understanding of the regulation of heparosan biosynthesis and may contribute to the study of other exopolysaccharide-producing strains.

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Draft Genome Sequence of Escherichia coli Strain Nissle 1917 (Serovar O6:K5:H1)

Cited by 31 publications

References 8 publications

Complete genome sequence of the Gram-negative probiotic Escherichia coli strain Nissle 1917

Complete genome sequence of the Gram-negative probiotic Escherichia coli strain Nissle 1917

Escherichia coli Isolate for Studying Colonization of the Mouse Intestine and Its Application to Two-Component Signaling Knockouts

Cyclic AMP (cAMP) Receptor Protein-cAMP Complex Regulates Heparosan Production in Escherichia coli Strain Nissle 1917

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