Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.592399
Title: Studies on the regulation of potassium efflux in Escherichia coli K12
Author: Elmore, M. J.
Awarding Body: University of Aberdeen
Current Institution: University of Aberdeen
Date of Award: 1992
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Abstract:
Aspects of the regulation of potassium efflux in Escherichia coli have been studied; in particular the mechanism by which NEM induces efflux. NEM induces efflux only in strains in which kefB and/or kefC are present. NEM-induced efflux via KefC is greater than via KefB, and the two gene products do not appear to interact. Mutant KefC alleles causing spontaneous efflux were studied. Plasmid-borne kefC+ allele can restore NEM-induced efflux to a strain lacking both kefB and kefC. NEM inhibits potassium uptake. An unc strain depleted of ATP by glucose starvation still gave NEM-induced efflux. Depletion by addition of iodoacetate inhibited NEM induced efflux but restoration of the ATP pool did not restore efflux. Similarly iodoacetate induced NEM-induced efflux in an ATP replete unc+ strain. Iodoacetate alone elicits slow potassium efflux. Addition of uncoupler did not inhibit the NEM effect. The NEM-induced efflux system can transport Rb+. The main target of NEM and iodoacetate is the intracellular glutathione pool; NEM does not elicit efflux in a glutathione-deficient strain unless glutathione is added exogenously. Reaction with iodoacetate (or a similar reagent) with glutathione prevents reaction of NEM with glutathione and hence the NEM effect. HPLC and TLC have been used to identify products of reaction of sulphydryl reagents with glutathione.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.592399  DOI: Not available
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