Remodelling of the Vibrio cholerae membrane by incorporation of exogenous fatty acids from host and aquatic environments.
Mol Microbiol. 2011 Feb; 79(3):716-28
Giles DK, Hankins JV, Guan Z, Trent MS.
Mol Microbiol. 2011 Feb; 79(3):716-28
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DiRita V and Matson J: F1000Prime Recommendation of [Giles DK et al., Mol Microbiol 2011, 79(3):716-28]. In F1000Prime, 07 Mar 2011; DOI: 10.3410/f.8468957.9290055. F1000Prime.com/8468957#eval9290055
F1000Prime Recommendations, Dissents and Comments for [Giles DK et al., Mol Microbiol 2011, 79(3):716-28]. In F1000Prime, 25 May 2013; F1000Prime.com/8468957
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The Gram-negative bacteria Vibrio cholerae poses significant public health concerns by causing an acute intestinal infection afflicting millions of people each year. V. cholerae motility, as well as virulence factor expression and outer membrane protein production, has been shown to be affected by bile. The current study examines the effects of bile on V. cholerae phospholipids. Bile exposure caused significant alterations to the phospholipid profile of V. cholerae but not of other enteric pathogens. These changes consisted of a quantitative increase and migratory difference in cardiolipin, decreases in phosphatidylglycerol and phosphatidylethanolamine, and the dramatic appearance of an unknown phospholipid determined to be lyso-phosphatidylethanolamine. Major components of bile were not responsible for the observed changes, but long-chain polyunsaturated fatty acids, which are minor components of bile, were shown to be incorporated into phospholipids of V. cholerae. Although the bile-induced phospholipid profile was independent of the V. cholerae virulence cascade, we identified another relevant environment in which V. cholerae assimilates unique fatty acids into its membrane phospholipids - marine sediment. Our results suggest that Vibrio species possess unique machinery conferring the ability to take up a wider range of exogenous fatty acids than other enteric bacteria.
© 2010 Blackwell Publishing Ltd.
DOI: 10.1111/j.1365-2958.2010.07476.x
PMID: 21255114
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