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Regulation of the Bacillus subtilis ccpC gene by CcpA and CcpC
Author(s) -
Kim HyunJin,
JourlinCastelli Cécile,
Kim SamIn,
Sonenshein Abraham L.
Publication year - 2002
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1046/j.1365-2958.2002.02751.x
Subject(s) - biology , ccpa , promoter , transcription factor , footprinting , transcription (linguistics) , gene , bacillus subtilis , transcriptional regulation , genetics , microbiology and biotechnology , gene expression , bacteria , linguistics , philosophy , catabolite repression , mutant
Summary Bacillus subtilis CcpC, a LysR‐type transcriptional regulator, represses the transcription of genes for citrate synthase ( citZ ) and aconitase ( citB ) in response to citrate availability. Transcription of ccpC was shown to initiate at two promoters, P1, located just upstream of the ccpC gene, and P2, located within or upstream of the neighbouring ykuL gene. Expression from the ccpC ‐specific promoter (P1) was negatively regulated by CcpC but independent of the carbon source in the medium. Gel shift and DNase I footprinting experiments revealed that CcpC binds to an interrupted dyad sequence that surrounds the ccpC transcriptional start point. Transcription of ccpC from the upstream promoter (P2) was repressed by glucose in a CcpA‐dependent manner. A putative CcpA binding site ( cre ) was identified upstream of the –35 region of the P1 promoter. Transcriptional fusion studies demonstrated that glucose repression of ccpC expression from the P2 promoter depends on this cre site. In addition, DNase I footprinting experiments showed that CcpA specifically binds to this cre site and that the introduction of mutations ( cre *) into this site abolished the binding. These results suggest that CcpA may control CcpC syn‐thesis by acting as a road‐block to readthrough transcription from the P2 promoter.