Difference between revisions of "CggR"

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(Expression and regulation)
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** The primary mRNAs of the operon are highly unstable. The primary mRNA is subject to processing at the very end of the ''[[cggR]]'' open reading frame. This results in stable mature ''[[gapA]]'' and ''[[gapA]]-[[pgk]]-[[tpiA]]-[[pgm]]-[[eno]]'' mRNAs. {{PubMed|11489127}}  The processing event requires the [[Rny|RNase Y]] {{PubMed|19193632}}.
 
** The primary mRNAs of the operon are highly unstable. The primary mRNA is subject to processing at the very end of the ''[[cggR]]'' open reading frame. This results in stable mature ''[[gapA]]'' and ''[[gapA]]-[[pgk]]-[[tpiA]]-[[pgm]]-[[eno]]'' mRNAs. {{PubMed|11489127}}  The processing event requires the [[Rny|RNase Y]] {{PubMed|19193632}}.
 
** The intracellular concentration of CggR is about 230 nM  (according to {{PubMed|20408793}}).
 
** The intracellular concentration of CggR is about 230 nM  (according to {{PubMed|20408793}}).
**  The accumulation of the ''[[cggR]]-[[gapA]]'' mRNA is strongly dependent on the presence of the [[YkzW]] peptide {{PubMed|20444087}}.
+
**  The accumulation of the ''[[cggR]]-[[gapA]]'' mRNA is strongly dependent on the presence of the [[YkzW]] peptide, due to stabilization of the mRNA {{PubMed|20444087}}.
  
 
=Biological materials =
 
=Biological materials =

Revision as of 12:31, 11 May 2010

Gene name cggR
Synonyms yvbQ
Essential no
Product central glycolytic genes regulator
Function transcriptional regulator
Metabolic function and regulation of this protein in SubtiPathways:
Central C-metabolism
MW, pI 37,2 kDa,5.68
Gene length, protein length 1020 bp, 340 amino acids
Immediate neighbours gapA, araE
Get the DNA and protein sequences
(Barbe et al., 2009)
Genetic context
CggR context.gif
This image was kindly provided by SubtiList








The gene

Basic information

  • Locus tag: BSU33950

Phenotypes of a mutant

Database entries

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

Additional information

The protein

Basic information/ Evolution

  • Catalyzed reaction/ biological activity: transcription repression of the glycolytic gapA operon
  • Protein family: sorC transcriptional regulatory family (according to Swiss-Prot)
  • Paralogous protein(s):

Extended information on the protein

  • Kinetic information:
  • Domains:
    • DNA binding domain (H-T-H motif) (37–56)
  • Modification:
  • Cofactor(s):
  • Effectors of protein activity: fructose 1.6-bisphosphate PubMed and dihydroxyacetone phosphate, glucose-6-phosphate and fructose-6-phosphate PubMed act as inducer and result in release of CggR from the DNA
  • Interactions:
    • active as dimer (according to PubMed)
  • Localization:

Database entries

  • Structure: 2OKG ( effector binding domain), 3BXH (in complex with fructose-6-phosphate), complex with Fructose-6-Phosphate NCBI, effector binding domain NCBI
  • KEGG entry: [3]

Additional information

Expression and regulation

  • Regulation:
    • expression activated by glucose (77-fold) (CggR) PubMed
  • Regulatory mechanism:
  • Additional information:
    • The primary mRNAs of the operon are highly unstable. The primary mRNA is subject to processing at the very end of the cggR open reading frame. This results in stable mature gapA and gapA-pgk-tpiA-pgm-eno mRNAs. PubMed The processing event requires the RNase Y PubMed.
    • The intracellular concentration of CggR is about 230 nM (according to PubMed).
    • The accumulation of the cggR-gapA mRNA is strongly dependent on the presence of the YkzW peptide, due to stabilization of the mRNA PubMed.

Biological materials

  • Expression vector: pGP705 (N-terminal His-tag, in pWH844), available in Stülke lab
  • GFP fusion:
  • Antibody: available in Stülke lab

Labs working on this gene/protein

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

Your additional remarks

References

Reviews

Sabine Brantl, Andreas Licht
Characterisation of Bacillus subtilis transcriptional regulators involved in metabolic processes.
Curr Protein Pept Sci: 2010, 11(4);274-91
[PubMed:20408793] [WorldCat.org] [DOI] (I p)


Original Publications