Difference between revisions of "RocG"

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(Phenotypes of a mutant)
(Phenotypes of a mutant)
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===Phenotypes of a mutant ===
 
===Phenotypes of a mutant ===
  
Poor growth on complex media such as LB. No growth in minimal media with arginine as the only carbon source. Rapid accumulation of suppressor mutants ([[gudB]] ''gudB1'')
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Poor growth on complex media such as LB. No growth in minimal media with arginine as the only carbon source. Rapid accumulation of suppressor mutants (gud |''gudB1'')
  
 
=== Database entries ===
 
=== Database entries ===

Revision as of 19:26, 18 December 2008

  • Description: write here

Gene name rocG
Synonyms
Essential no
Product glutamate dehydrogenase (major)
Function arginine utilization, controls the activity of GltC
MW, pI 46.2 kDa, 6.28
Gene length, protein length 1272 bp, 424 amino acids
Immediate neighbours yweA, rocA
Gene sequence (+200bp) Protein sequence
Genetic context
File:GenE context.gif












The gene

Basic information

  • Coordinates:

Phenotypes of a mutant

Poor growth on complex media such as LB. No growth in minimal media with arginine as the only carbon source. Rapid accumulation of suppressor mutants (gud |gudB1)

Database entries

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

Additional information

The protein

Basic information/ Evolution

  • Catalyzed reaction/ biological activity: L-glutamate + H(2)O + NAD(+) = 2-oxoglutarate + NH(3) + NADH
  • Protein family: Glu/Leu/Phe/Val dehydrogenases family
  • Paralogous protein(s): GudB

Extended information on the protein

  • Kinetic information:
  • Domains:
  • Modification:
  • Cofactor(s):
  • Effectors of protein activity:
  • Interactions: RocG-GltC
  • Localization:

Database entries

  • Structure:
  • Swiss prot entry: [3]
  • KEGG entry: [4]
  • E.C. number: [5]

Additional information

Expression and regulation

  • Operon: rocG
  • Regulation: induced by arginine (RocR, AhrC), ornithine or proline, subject to carbon catabolite repression (CcpA)
  • Regulatory mechanism: RocR: transcription activation; AhrC: transcription activation; CcpA: transcription repression
  • Additional information:

Biological materials

Labs working on this gene/protein

Linc Sonenshein, Tufts University, Boston, MA, USA Homepage

Jörg Stülke, University of Göttingen, Germany Homepage

Your additional remarks

References

  1. Author1, Author2 & Author3 (year) Title Journal volume: page-page. PubMed