Regulation of fatty acid biosynthesis by the global regulator CcpA and the local regulator FabT in Streptococcus mutans
Summary SMU.1745c, encoding a putative transcriptional regulator of the MarR family, maps to a location proximal to the fab gene cluster in Streptococcus mutans. Deletion of the SMU.1745c (fabTSm) coding region resulted in a membrane fatty acid composition comprised of longer‐chained, unsaturated fa...
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Published in: | Molecular oral microbiology Vol. 30; no. 2; pp. 128 - 146 |
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Main Authors: | , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Denmark
Blackwell Publishing Ltd
01-04-2015
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Subjects: | |
Online Access: | Get full text |
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Summary: | Summary
SMU.1745c, encoding a putative transcriptional regulator of the MarR family, maps to a location proximal to the fab gene cluster in Streptococcus mutans. Deletion of the SMU.1745c (fabTSm) coding region resulted in a membrane fatty acid composition comprised of longer‐chained, unsaturated fatty acids (UFA), compared with the parent strain. Previous reports have indicated a role for FabT in regulation of genes in the fab gene cluster in other organisms, through binding to a palindromic DNA sequence. Consensus FabT motif sequences were identified in S. mutans in the intergenic regions preceding fabM, fabTSm and fabK in the fab gene cluster. Chloramphenicol acetyltransferase (cat) reporter fusions, using the fabM promoter, revealed elevated transcription in a ∆fabTSm background. Transcription of fabTSm was dramatically elevated in cells grown at pH values of 5 and 7 in the ∆ fabTSm background. Transcription of fabTSm was also elevated in a strain carrying a deletion for the carbon catabolite repressor CcpA. Purified FabTSm and CcpA bound to the promoter regions of fabTSm and fabM. Hence, the data indicate that FabTSm acts as a repressor of fabM and fabTSm itself and the global regulator CcpA acts as a repressor for fabTSm. |
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Bibliography: | istex:778607C2D271BEDF3342F20AA83FA1E8A6FD1597 ark:/67375/WNG-037VXLZD-X ArticleID:OMI12076 NIH/NIDCR - No. DE-13683; No. DE017425; No. DE017157; No. T32 DE-07165; No. T90-DE021985 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These authors contributed equally. |
ISSN: | 2041-1006 2041-1014 |
DOI: | 10.1111/omi.12076 |