Format

Send to

Choose Destination
Proteome Sci. 2010 Jun 25;8:37. doi: 10.1186/1477-5956-8-37.

Identification of proteins related to the stress response in Enterococcus faecalis V583 caused by bovine bile.

Author information

1
Department of Chemistry, Biotechnology and Food Science, Norwegian University of Life Sciences, Chr, M, Falsensvei 1, N-1432 As, Norway. geir.mathiesen@umb.no.

Abstract

BACKGROUND:

Enterococcus faecalis is an opportunistic pathogen and one of the most important causes of hospital infections. Bile acids are a major stress factor bacteria have to cope with in order to colonize and survive in the gastro-intestinal tract. The aim of this study was to investigate the effects of bile acids on the intracellular proteome of E. faecalis V583.

RESULTS:

The proteomes of cells challenged with 1% bile were analyzed after 20 - 120 minutes exposure, using 2D gel electrophoresis and mass spectrometry. Among the approximately 500 observed proteins, 53 unique proteins were found to be regulated in response to bile and were identified with mass spectrometry. The identified proteins belonged to nine different functional classes, including fatty acid- and phospholipid-biosynthesis, energy metabolism, and transport and binding. Proteins involved in fatty acid and phospholipid biosynthesis pathways were clearly overrepresented among the identified proteins and all were down-regulated upon exposure to bile. The proteome data correlated reasonably well with data from previous transcriptome experiments done under the same conditions, but several differences were observed.

CONCLUSION:

The results provide an overview of potentially important proteins that E. faecalis V583 needs to regulate in order to survive and adapt to a bile-rich environment, among which are several proteins involved in fatty acid and phospholipid biosynthesis pathways. In addition, this study reveals several hypothetical proteins, which are both abundant and clearly regulated and thus stand out as targets for future studies on bile stress.

Supplemental Content

Full text links

Icon for BioMed Central Icon for PubMed Central
Loading ...
Support Center