title: Two different mechanisms mediate catabolite repression of the Bacillus subtilis levanase operon.
abstract: There are two levels of control of the expression of the levanase operon in Bacillus subtilis: induction by fructose, which involves a positive regulator, LevR, and the fructose phosphotransferase system encoded by this operon (lev-PTS), and a global regulation, catabolite repression. The LevR activator interacts with its target, the upstream activating sequence (UAS), to stimulate the transcription of the E sigma L complex bound at the "-12, -24" promoter. Levanase operon expression in the presence of glucose was tested in strains carrying a ccpA gene disruption or a ptsH1 mutation in which Ser-46 of HPr is replaced by Ala. In a levR+ inducible genetic background, the expression of the levanase operon was partially resistant to catabolite repression in both mutants, indicating that the CcpA repressor and the HPr-SerP protein are involved in the glucose control of this operon. In addition, a cis-acting catabolite-responsive element (CRE) of the levanase operon was identified and investigated by site-directed mutagenesis. The CRE sequence TGAAAACGCTT(a)ACA is located between positions -50 and -36 from the transcriptional start site, between the UAS and the -12, -24 promoter. However, in a background constitutive for levanase, neither HPr, CcpA, nor CRE is involved in glucose repression, suggesting the existence of a different pathway of glucose regulation. Using truncated LevR proteins, we showed that this CcpA-independent pathway required the presence of the domain of LevR (amino acids 411 to 689) homologous to the BglG family of bacterial antiterminators.
authors.affiliation: Unité de Biochimie Microbienne, Institut Pasteur, URA 1300 du Centre National de la Recherche Scientifique, Paris, France.
authors.forename: I
authors.initials: I
authors.lastname: Martin-Verstraete
authors.forename: J
authors.initials: J
authors.lastname: Stülke
authors.forename: A
authors.initials: A
authors.lastname: Klier
authors.forename: G
authors.initials: G
authors.lastname: Rapoport
mesh_terms: D001412:Bacillus subtilis / Q000201:enzymology / Q000235:genetics*; D001426:Bacterial Proteins / Q000235:genetics; D001483:Base Sequence; D004268:DNA-Binding Proteins / Q000378:metabolism; D004790:Enzyme Induction; D004794:Enzyme Repression; D015964:Gene Expression Regulation, Bacterial; D005798:Genes, Bacterial; D005947:Glucose / Q000494:pharmacology; D006026:Glycoside Hydrolases / Q000235:genetics*; D008957:Models, Genetic; D008969:Molecular Sequence Data; D009154:Mutation; D009876:Operon; D010731:Phosphoenolpyruvate Sugar Phosphotransferase System / Q000378:metabolism; D012045:Regulatory Sequences, Nucleic Acid; D012097:Repressor Proteins / Q000378:metabolism; D017384:Sequence Deletion; D015398:Signal Transduction; D014157:Transcription Factors / Q000235:genetics
chemical_list: D001426:Bacterial Proteins; D004268:DNA-Binding Proteins; D012097:Repressor Proteins; D014157:Transcription Factors; C069286:catabolite control proteins, bacteria; C067962:LevR protein, Bacillus subtilis; D010731:Phosphoenolpyruvate Sugar Phosphotransferase System; C030182:phosphocarrier protein HPr; D006026:Glycoside Hydrolases; C021512:levanase; D005947:Glucose