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Glucose Transport in Brucella abortus
Journal article   Open access   Peer reviewed

Glucose Transport in Brucella abortus

Richard F. Rest and Donald C. Robertson
Journal of bacteriology, v 118(1)
01 Apr 1974
PMID: 4206873
url
https://doi.org/10.1128/jb.118.1.250-258.1974View
Published, Version of Record (VoR)Maybe Open Access (Publisher Bronze) Open
url
https://doi.org/10.1128/JB.118.1.250-258.1974View
Published, Version of Record (VoR) Open

Abstract

Physiology and Metabolism
Brucella abortus British strain 19 transported glucose with an apparent K m of 0.16 mM and an apparent V max of 250 nmol per min per mg of N. The only common glucose analogue transported was 2-deoxyglucose (2-DOG), with an apparent K i of 0.73 mM. Alpha- or beta-methyl glucosides and 3- O -methylglucose were not transported. Transport was linear for 70 to 90 s, depending on the concentration of substrate used. 2-Deoxyglucose was transported as the free sugar and was not further metabolized once inside the cell. There was no glucose phosphoenolpyruvate phosphotransferase system (PEP-PTS) present, and there were no inhibitors present in Brucella cell-free extract that inhibited the Escherichia coli glucose PEP-PTS. N -Ethylmaleimide (NEM) and p -chloromercuribenzoate ( p CMB) completely inhibited transport of glucose and 2-DOG. Glutathione, dithiothreitol, and β-mercaptoethanol reversed the effects of p CMB but not of NEM. A pH optimum of 7.2 and a temperature optimum of 37 to 45 C were observed for both K m and V max . The glucose transport system appeared to be constitutive for glucose transport in cells grown on fructose, galactose, erythritol, or glucose. The electron transfer inhibitors carbonyl cyanide, m -chlorophenylhydrazone, NaN 3 , 2,4-dinitrophenol, and KCN inhibited 2-DOG transport to a greater extent than did the metabolic energy inhibitors NaAsO 4 , iodoacetate, KF, and 2-heptyl-4-hydroxyquinoline- N -oxide. Dicyclohexylcarbodiimide, an inhibitor of membrane-bound adenosine triphosphatases, inhibited transport by 100%.

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