CcpN

From SubtiWiki
Revision as of 12:15, 11 June 2009 by CLammers (talk | contribs)
Jump to: navigation, search
  • Description: transcriptional repressor of gluconeogenetic genes and of sr1. repression in the presence of glucose

Gene name ccpN
Synonyms yqzB
Essential no
Product transcriptional regulator
Function repressor of genes involved in
gluconeogenesis (gapB, pckA) and of sr1
Metabolic function and regulation of this protein in SubtiPathways:
Central C-metabolism
MW, pI 23.4 kDa, 7.22
Gene length, protein length 636 bp, 212 amino acids
Immediate neighbours yqfL, glyS
Get the DNA and protein sequences
(Barbe et al., 2009)
Genetic context
YqzB context.gif
This image was kindly provided by SubtiList





The gene

Basic information

  • Locus tag: BSU25250

Phenotypes of a mutant

Impaired growth on glucose due to re-routing of carbon from glycolysis to the pentose phosphate pathway PubMed

Database entries

  • DBTBS entry: [1]
  • SubtiList entry: [2]

Additional information

The protein

Basic information/ Evolution

  • Catalyzed reaction/ biological activity: transcription repression of the gapB, pckA, and sr1 genes in the presence of glucose PubMed
  • Protein family:
  • Paralogous protein(s):

Extended information on the protein

  • Kinetic information:
  • Domains:
  • Modification:
  • Cofactor(s):
  • Effectors of protein activity:
    • YqfL (negative effector of CcpN activity) PubMed
    • ATP enhances CcpN-dependent repression, ADP counteracts the repressing activity of CcpN PubMed
  • Interactions:
  • Localization:

Database entries

  • Structure:
  • KEGG entry: [3]

Additional information

Expression and regulation

  • Regulation: constitutively expressed PubMed
  • Additional information:

Biological materials

  • Expression vector:
  • lacZ fusion:
  • GFP fusion:

Labs working on this gene/protein

Stephane Aymerich, Microbiology and Molecular Genetics, INRA Paris-Grignon, France

Sabine Brantl, Bacterial Genetics, Friedrich-Schiller-University of Jena, Germany homepage

Uwe Sauer, ETH Zürich, Switzerland homepage

Your additional remarks

References

Simon Tännler, Eliane Fischer, Dominique Le Coq, Thierry Doan, Emmanuel Jamet, Uwe Sauer, Stéphane Aymerich
CcpN controls central carbon fluxes in Bacillus subtilis.
J Bacteriol: 2008, 190(18);6178-87
[PubMed:18586936] [WorldCat.org] [DOI] (I p)

Andreas Licht, Ralph Golbik, Sabine Brantl
Identification of ligands affecting the activity of the transcriptional repressor CcpN from Bacillus subtilis.
J Mol Biol: 2008, 380(1);17-30
[PubMed:18511073] [WorldCat.org] [DOI] (I p)

Andreas Licht, Sabine Brantl
Transcriptional repressor CcpN from Bacillus subtilis compensates asymmetric contact distribution by cooperative binding.
J Mol Biol: 2006, 364(3);434-48
[PubMed:17011578] [WorldCat.org] [DOI] (P p)

Andreas Licht, Sven Preis, Sabine Brantl
Implication of CcpN in the regulation of a novel untranslated RNA (SR1) in Bacillus subtilis.
Mol Microbiol: 2005, 58(1);189-206
[PubMed:16164558] [WorldCat.org] [DOI] (P p)

Pascale Servant, Dominique Le Coq, Stéphane Aymerich
CcpN (YqzB), a novel regulator for CcpA-independent catabolite repression of Bacillus subtilis gluconeogenic genes.
Mol Microbiol: 2005, 55(5);1435-51
[PubMed:15720552] [WorldCat.org] [DOI] (P p)


  1. Servant et al. (2005) CcpN (YqzB), a novel regulator for CcpA-independent catabolite repression of Bacillus subtilis gluconeogenic genes. Mol. Microbiol. 55: 1435-1451. PubMed
  2. Licht et al. (2005) Implication of CcpN in the regulation of a novel untranslated RNA (SR1) in Bacillus subtilis. Mol. Microbiol. 58: 189-206. PubMed
  3. Licht & Brantl (2006) Transcriptional repressor CcpN from Bacillus subtilis compensates asymmetric contact distribution by cooperative binding. J. Mol. Biol. 364: 434-448. PubMed
  4. Licht et al. (2008) Identification of ligands affecting the activity of the transcriptional repressor CcpN from Bacillus subtilis. J. Mol. Biol. 380: 17-30. PubMed
  5. Tännler et al. (2008) CcpN controls central carbon fluxes in Bacillus subtilis. J. Bacteriol. 190: 6178-6187. PubMed