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Long‐chain acyl‐acyl carrier protein activates transcriptional regulation of fatty acid biosynthesis in Streptococcus pneumoniae
Author(s) -
Jerga Agoston,
Rock Charles O
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.689.11
Subject(s) - acyl carrier protein , repressor , biochemistry , promoter , gene , electrophoretic mobility shift assay , biosynthesis , transcription (linguistics) , transcriptional regulation , fatty acid , chemistry , biology , dna , gene expression , enzyme , microbiology and biotechnology , linguistics , philosophy
In the human pathogen S. pneumoniae , transcription of the fab genes encoding the enzymes of type II fatty acid biosynthesis is controlled by FabT, a transcriptional repressor. However, FabT overexpression fails to suppress fab gene expression indicating that a metabolic signal in addition to FabT is required for transcriptional regulation. A screen of metabolic intermediates for their effect on FabT DNA binding revealed that long‐chain acyl‐acyl carrier protein (ACP) end‐products of fatty acid synthesis increased FabT binding to specific sites within the promoters of the fab genes. Activation of FabT DNA binding was most prominent in the presence of acyl‐ACPs carrying either saturated or unsaturated fatty acids of 16 to 18 carbon chain length. Electrophoresis mobility shift assay confirmed that acyl‐ACP binds to FabT and forms a FabT‐acyl‐ACP‐DNA complex. Thus, the transcription of the fab genes is controlled by a feedback regulatory loop involving the binding of acyl‐ACP end products of fatty acid biosynthesis to FabT that increases its affinity for specific sites within the fab promoters thereby repressing fab gene expression. (Supported by NIH GM34496 and ALSAC)