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Title: A physiological function for the KEFB and KEFC systems of Escherichia coli in protection against methylglyoxal
Author: Ferguson, Gail P.
ISNI:       0000 0001 2412 0400
Awarding Body: University of Aberdeen
Current Institution: University of Aberdeen
Date of Award: 1994
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The work presented investigates the physiological function of the Escherichia coli potassium efflux systems, KefB and KefC. We have found that these systems are activated during the glutathione-dependent metabolism of the naturally-occurring electrophile, methylglyoxal. KefB was found to be the major system involved; the KefC system was found only to play a minor role. We proposed that one or both of the glutathione metabolites, hemithiolacetal and S-lactoylglutathione, formed during the glutathione-dependent metabolism of methylglyoxal is an activator of the KefB and KefC systems. The activation and activity of the KefB and KefC systems was found to protect cells against methylglyoxal. Cells that lack the KefB and KefC systems or cells that are unable to release potassium, by the KefB and KefC systems, due to the presence of external potassium exhibit a drastically-increased sensitivity towards methylglyoxal. The KefB and KefC systems afford protection against both exogenously-added and endogenously-synthesized methylglyoxal. However, these systems only delay the onset of the death phase against the continuous production of endogenously-synthesized methylglyoxal. Consistent with the efflux data, KefB was found to be the major system involved in the protection, although the KefC system did confer some limited protection. Thus, we proposed that the KefB and KefC systems have a physiological function in the protection of cells against naturally-produced methylglyoxal. The exact mechanism by which the KefB and KefC systems confer protection against methylglyoxal is at present unknown. Preliminary weak acid experiments have provided strong evidence that if potassium release by the KefB and KefC systems is accompanied by acidification of the cytoplasm then acidification might be responsible for part or all of the protection observed.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available
Keywords: Genetics