Glucose uptake by Listeria monocytogenes Scott A and inhibition by pediocin JD

Glucose uptake by Listeria monocytogenes Scott A was inhibited by the bacteriocin pediocin JD and by the protonophore carbonyl cyanide m-chlorophenyhydrazone. Experiments with monensin, nigericin, chlorhexidine diacetate, dinitrophenol, and gramicidin, however, showed that glucose uptake could occur...

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Published inApplied and Environmental Microbiology Vol. 60; no. 10; pp. 3870 - 3873
Main Authors Christensen, D.P, Hutkins, R.W
Format Journal Article
LanguageEnglish
Published Washington, DC American Society for Microbiology 01.10.1994
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Summary:Glucose uptake by Listeria monocytogenes Scott A was inhibited by the bacteriocin pediocin JD and by the protonophore carbonyl cyanide m-chlorophenyhydrazone. Experiments with monensin, nigericin, chlorhexidine diacetate, dinitrophenol, and gramicidin, however, showed that glucose uptake could occur in the absence of a proton motive force. L. monocytogenes cell extracts phosphorylated glucose when phosphoenolpyruvate (PEP) was present in the assay mixture, and whole cells incubated with 2-deoxyglucose accumulated 2-deoxyglucose-6-phosphate, indicating the presence of a PEP-dependent phosphotransferase system in this organism. Glucose phosphorylation also occurred when ATP was present, suggesting that a proton motive force-mediated glucose transport system may also be present. We conclude that L. monocytogenes Scott A accumulates glucose by phosphotransferase and proton motive force-mediated systems, both of which are sensitive to pediocin JD
Bibliography:Q03
9519018
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ISSN:0099-2240
1098-5336
DOI:10.1128/aem.60.10.3870-3873.1994