Document Detail


The Vibrio cholerae fatty acid regulatory protein, FadR, represses transcription of plsB, the gene encoding the first enzyme of membrane phospholipid biosynthesis.
MedLine Citation:
PMID:  21771112     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Glycerol-3-phosphate (sn-glycerol-3-P, G3P) acyltransferase catalyses the first committed step in the biosynthesis of membrane phospholipids, the acylation of G3P to form 1-acyl G3P (lysophosphatidic acid). The paradigm G3P acyltransferase is the Escherichia coli plsB gene product which acylates position-1 of G3P using fatty acids in thioester linkage to either acyl carrier protein (ACP) or CoA as acyl donors. Although the E. coli plsB gene was discovered about 30 years ago, no evidence for transcriptional control of its expression has been reported. However A.E. Kazakov and co-workers (J Bacteriol 2009; 191: 52-64) reported the presence of a putative FadR binding site upstream of the candidate plsB genes of Vibrio cholerae and three other Vibrio species suggesting that plsB might be regulated by FadR, a GntR family transcription factor thus far known only to regulate fatty acid synthesis and degradation. We report that the V. cholerae plsB homologue restored growth of E. coli strain BB26-36 which is a G3P auxotroph due to an altered G3P acyltransferase activity. The plsB promoter was also mapped and the predicted FadR-binding palindrome was found to span positions -19 to -35, upstream of the transcription start site. Gel shift assays confirmed that both V. cholerae FadR and E. coli FadR bound the V. cholerae plsB promoter region and binding was reversed upon addition of long-chain fatty acyl-CoA thioesters. The expression level of the V. cholerae plsB gene was elevated two- to threefold in an E. coli fadR null mutant strain indicating that FadR acts as a repressor of V. cholerae plsB expression. In both E. coli and V. cholerae the β-galactosidase activity of transcriptional fusions of the V. cholerae plsB promoter to lacZ increased two- to threefold upon supplementation of growth media with oleic acid. Therefore, V. cholerae co-ordinates fatty acid metabolism with 1-acyl G3P synthesis.
Authors:
Youjun Feng; John E Cronan
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2011-07-19
Journal Detail:
Title:  Molecular microbiology     Volume:  81     ISSN:  1365-2958     ISO Abbreviation:  Mol. Microbiol.     Publication Date:  2011 Aug 
Date Detail:
Created Date:  2011-08-11     Completed Date:  2011-12-02     Revised Date:  2012-04-04    
Medline Journal Info:
Nlm Unique ID:  8712028     Medline TA:  Mol Microbiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  1020-33     Citation Subset:  IM    
Copyright Information:
© 2011 Blackwell Publishing Ltd.
Affiliation:
Department of Microbiology, University of Illinois, Urbana, IL 61801, USA.
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MeSH Terms
Descriptor/Qualifier:
Acetyltransferases / antagonists & inhibitors,  biosynthesis*
Amino Acid Sequence
Artificial Gene Fusion
Bacterial Proteins / metabolism*
Base Sequence
Binding Sites
Biosynthetic Pathways / genetics
Electrophoretic Mobility Shift Assay
Escherichia coli / genetics,  metabolism
Gene Expression Profiling
Gene Expression Regulation, Bacterial*
Genes, Reporter
Models, Biological
Molecular Sequence Data
Phospholipids / metabolism*
Promoter Regions, Genetic
Protein Binding
Repressor Proteins / metabolism*
Transcription, Genetic*
Vibrio cholerae / genetics*
beta-Galactosidase / genetics,  metabolism
Grant Support
ID/Acronym/Agency:
AI15650/AI/NIAID NIH HHS; R01 AI015650-35/AI/NIAID NIH HHS; R01 AI015650-36/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/Bacterial Proteins; 0/FadR protein, Bacteria; 0/Phospholipids; 0/Repressor Proteins; EC 2.3.1.-/Acetyltransferases; EC 3.2.1.23/beta-Galactosidase

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


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