Similarity to peroxisomal-membrane protein family reveals that Sinorhizobium and Brucella BacA affect lipid-A fatty acids

ECU Author/Contributor (non-ECU co-authors, if there are any, appear on document)
John Baumgartner (Creator)
Russ W. Carlson (Creator)
Anup Datta (Creator)
Gail P. Ferguson (Creator)
R. Martin II Roop (Creator)
Graham C. Walker (Creator)
Institution
East Carolina University (ECU )
Web Site: http://www.ecu.edu/lib/

Abstract: Sinorhizobium meliloti a legume symbiont and Brucella abortus a phylogenetically related mammalian pathogen both require the bacterial-encoded BacA protein to establish chronic intracellular infections in their respective hosts. We found that the bacterial BacA proteins share sequence similarity with a family of eukaryotic peroxisomal-membrane proteins including the human adrenoleukodystrophy protein required for the efficient transport of verylong- chain fatty acids out of the cytoplasm. This insight along with the increased sensitivity of BacA-deficient mutants to detergents and cell envelope-disrupting agents led us to discover that BacA affects the very-long-chain fatty acid (27-OHC28:0 and 29-OHC30:0) content of both Sinorhizobium and Brucella lipid A. We discuss models for how BacA function affects the lipid-A fatty-acid content and why this activity could be important for the establishment of chronic intracellular infections. Originally published Proceedings of the National Academy of Sciences Vol. 101 No. 14 Apr 2004

Additional Information

Publication
Other
Proceedings of the National Academy of Sciences. 101:14(April 2004) p. 5012-5017.
Language: English
Date: 2011
Keywords
Sinorhizobium meliloti, Brucella abortus, BacA protein, lipid fatty acid

Email this document to

This item references:

TitleLocation & LinkType of Relationship
Similarity to peroxisomal-membrane protein family reveals that Sinorhizobium and Brucella BacA affect lipid-A fatty acidshttp://hdl.handle.net/10342/3258The described resource references, cites, or otherwise points to the related resource.