Document Detail


Cyclopropane fatty acids improve Escherichia coli survival in acidified minimal media by reducing membrane permeability to H+ and enhanced ability to extrude H+.
MedLine Citation:
PMID:  18562182     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The physiological role of cyclopropane fatty acids (CFAs) in acid stress resistance was studied by in situ microelectrode H+ flux measurements of Escherichia coli Frag1 and its isogenic CFA-deficient mutant JBM 1. After exposure to pH 4 for 16h, net H+ influx in JBM 1 was twice that of the parent strain. H+ flux stabilisation at pH 6 after acid stress took more time in the cfa- mutant. The data suggest increased proton permeability and decreased ability to extrude H+ in the absence of CFA, and they support the hypothesis that CFAs protect E. coli in acidic environments by decreasing membrane permeability to H+.
Authors:
Lana Shabala; Tom Ross
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-05-09
Journal Detail:
Title:  Research in microbiology     Volume:  159     ISSN:  0923-2508     ISO Abbreviation:  Res. Microbiol.     Publication Date:    2008 Jul-Aug
Date Detail:
Created Date:  2008-08-25     Completed Date:  2008-11-06     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8907468     Medline TA:  Res Microbiol     Country:  France    
Other Details:
Languages:  eng     Pagination:  458-61     Citation Subset:  IM    
Affiliation:
Food Safety Centre, Tasmanian Institute of Agricultural Research, School of Agricultural Science, University of Tasmania, Private Bag 54, Hobart, Tas 7001, Australia.
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MeSH Terms
Descriptor/Qualifier:
Acids / metabolism*
Cell Membrane Permeability*
Culture Media / chemistry*
Cyclopropanes / metabolism*
Escherichia coli / growth & development*,  metabolism*
Fatty Acids / metabolism*
Hydrogen-Ion Concentration
Microbial Viability
Protons
Chemical
Reg. No./Substance:
0/Acids; 0/Culture Media; 0/Cyclopropanes; 0/Fatty Acids; 0/Protons; 0/cyclopropane fatty acids

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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