Kevin Matthew McKay Week 5

From OpenWetWare


  • GDH1
    • Expression is regulated by carbon sources
      • High expression in presence of glucose and ethanol
  • GDH3
    • Expression regulated by carbon sources
      • High expression in presence of ethanol, repressed by glucose
  • GDH2
    • Homo Sapien Homolog:
      • GLUD2 and GLUD1
        • Deficiency has been linked to hyperinsulinism-hyperammonemia syndrome and various neurological disorders.
    • Expression regulated by nitrogen catabolite repression and intracellular ammonia levels
    • Also regulated through transcription in the promoter
  • GLN1
    • Expression regulated by nitrogen source and amino acid limitation
  • GLT1
    • Expression regulated by glutamate-mediated repression and GLN3P/GCN4P-mediated activation, availability of nitrogen and glutamate, and when amino acids are limiting, GLT1 expression is activated by GCN4P.
  • Parameters related to our chemostat model were found in many of the papers related to these five genes including amounts of nutrients carbon and nitrogen (carbon being held constant in the ter shure paper), flux rate, (which was also held constant in the ter shure paper).

KEGG Pathway

  • Central Nitrogen Metabolism
  • All pf the genes in the reference pathway are in the yeast pathway on the website
  • The KEGG website gave the amino acid and nucleotide sequences of the genes while the other website did not


  • The reactome website was hard to use, after searching for quite some time I was able to find the part of our pathway where glutamate is converted back into glutamine by the addition of nitrogen in the form of ammonium. Reactome did not provide the gene involoved (GLN1) or the enzyme (GS), it did show that one ATP was dephosphorylated.
  • Glutamate to Glutamine