Identification of the AraE transport protein of <i>Escherichia coli</i>

Macpherson, Andrew J.; Jones‐Mortimer, M. C.; Henderson, Peter J. F.

doi:10.1042/bj1960269

Cited by 52 publications

(35 citation statements)

References 45 publications

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“…Inclusion of this mutation also prevents breakdown of arabinose retained in the cell cytoplasm at the time of oral immunization, and inclusion of the ⌬araE25 mutation (Fig. 1j) that enhances retention of arabinose (35,48) further delays cessation in expression of araC P BAD -regulated genes for an additional cell division or so. The suicide vectors for introducing the ⌬araBAD23 and ⌬araE25 mutations are listed in Table 2.…”

Section: Resultsmentioning

confidence: 99%

Salmonella entericaSerovar Typhimurium Strains with Regulated Delayed Attenuation In Vivo

et al. 2009

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Recombinant bacterial vaccines must be fully attenuated for animal or human hosts to avoid inducing disease symptoms while exhibiting a high degree of immunogenicity. Unfortunately, many well-studied means for attenuating Salmonella render strains more susceptible to host defense stresses encountered following oral vaccination than wild-type virulent strains and/or impair their ability to effectively colonize the gut-associated and internal lymphoid tissues. This thus impairs the ability of recombinant vaccines to serve as factories to produce recombinant antigens to induce the desired protective immunity. To address these problems, we designed strains that display features of wild-type virulent strains of Salmonella at the time of immunization to enable strains first to effectively colonize lymphoid tissues and then to exhibit a regulated delayed attenuation in vivo to preclude inducing disease symptoms. We recently described one means to achieve this based on a reversible smooth-rough synthesis of lipopolysaccharide O antigen. We report here a second means to achieve regulated delayed attenuation in vivo that is based on the substitution of a tightly regulated araC P BAD cassette for the promoters of the fur, crp, phoPQ, and rpoS genes such that expression of these genes is dependent on arabinose provided during growth. Thus, following colonization of lymphoid tissues, the Fur, Crp, PhoPQ, and/or RpoS proteins cease to be synthesized due to the absence of arabinose such that attenuation is gradually manifest in vivo to preclude induction of diseases symptoms. Means for achieving regulated delayed attenuation can be combined with other mutations, which together may yield safe efficacious recombinant attenuated Salmonella vaccines.

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Section: Resultsmentioning

confidence: 99%

Salmonella entericaSerovar Typhimurium Strains with Regulated Delayed Attenuation In Vivo

et al. 2009

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“…Similarly, EjIMan (ptsM) is able to recognize, transport, and phosphorylate glucose (21,73). Glucose can also be taken up without chemical alteration by at least two active transport systems: one is the proton motive force (PMF)-dependent galactose transport system (galP) (37). Glucose is not an inducer of the GalP transport system.…”

Section: Discussionmentioning

confidence: 99%

The malX malY operon of Escherichia coli encodes a novel enzyme II of the phosphotransferase system recognizing glucose and maltose and an enzyme abolishing the endogenous induction of the maltose system

Reidl

Boos

1991

J Bacteriol

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Mutants lacking MalK, a subunit of the binding protein-dependent maltose-maltodextrin transport system, constitutively express the maltose genes. A second site mutation in mall abolishes the constitutive expression. glucose in a ptsM ptsG glk mutant, and the plasmid-encoded MalY alone was sufficient to abolish the constitutivity of the mal genes in a malK mutant. The overexpressio'n of malY in a strain that is wild type with respect to the maltose genes strongly interferes with growth on maltose. This is not the case in a malT(Con) strain that expresses the mal genes constitutively. We conclude that malY encodes an enzyme that degrades the inducer of the maltose system or prevents its synthesis.

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“…Our data show that inducer exclusion regulates the activity of an S. Typhimurium transporter of a substrate available inside macrophages, which could include lactose, melibiose, and glucose/galactose (33,35,37). In the case of glucose and galactose, the inducer exclusion-dependent transporter is galactose permease (GalP) (2,29,30,33). GalP also transports glucose (39), and its expression is induced by availability of galactose (7).…”

Section: Glycolysis Is Required For Intracellular Replication and Surmentioning

confidence: 99%

Glucose and Glycolysis Are Required for the Successful Infection of Macrophages and Mice by Salmonella enterica Serovar Typhimurium

et al. 2009

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Salmonella is a widespread zoonotic enteropathogen that causes gastroenteritis and fatal typhoidal disease in mammals. During systemic infection of mice, Salmonella enterica serovar Typhimurium resides and replicates in macrophages within the "Salmonella-containing vacuole" (SCV). It is surprising that the substrates and metabolic pathways necessary for growth of S. Typhimurium within the SCV of macrophages have not been identified yet. To determine whether S. Typhimurium utilized sugars within the SCV, we constructed a series of S. Typhimurium mutants that lacked genes involved in sugar transport and catabolism and tested them for replication in mice and macrophages. These mutants included a mutant with a mutation in the pfkAB-encoded phosphofructokinase, which catalyzes a key committing step in glycolysis. We discovered that a pfkAB mutant is severely attenuated for replication and survival within RAW 264.7 macrophages. We also show that disruption of the phosphoenolpyruvate:carbohydrate phosphotransferase system by deletion of the ptsHI and crr genes reduces S. Typhimurium replication within RAW 264.7 macrophages. We discovered that mutants unable to catabolize glucose due to deletion of ptsHI, crr, and glk or deletion of ptsG, manXYZ, and glk showed reduced replication within RAW 264.7 macrophages. This study proves that S. Typhimurium requires glycolysis for infection of mice and macrophages and that transport of glucose is required for replication within macrophages.

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Identification of the AraE transport protein of Escherichia coli

Cited by 52 publications

References 45 publications

Salmonella entericaSerovar Typhimurium Strains with Regulated Delayed Attenuation In Vivo

Salmonella entericaSerovar Typhimurium Strains with Regulated Delayed Attenuation In Vivo

The malX malY operon of Escherichia coli encodes a novel enzyme II of the phosphotransferase system recognizing glucose and maltose and an enzyme abolishing the endogenous induction of the maltose system

Glucose and Glycolysis Are Required for the Successful Infection of Macrophages and Mice by Salmonella enterica Serovar Typhimurium

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