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Gene Review

GAT1  -  Gat1p

Saccharomyces cerevisiae S288c

Synonyms: MEP80, NIL1, Transcriptional regulatory protein GAT1, YFL021W
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High impact information on GAT1

  • Here we demonstrate a potentially general and scalable method of identifying such molecules by application to a particular protein, Ure2p, which represses the transcription factors Gln3p and Nil1p [1].
  • This transcriptional response is partly mediated by the nutrient-sensitive transcription factors GLN3 and NIL1 (also named GAT1) [2].
  • The results further indicate that Gln3p is inactivated by an increase in the intracellular concentration of glutamine and that Nil1p is inactivated by an increase in intracellular glutamate [3].
  • In contrast, expression of either MEP1 or MEP3 requires only Gln3p and is unexpectedly down-regulated in a Nil1p-dependent manner [4].
  • High-level MEP2 transcription requires at least one of the two GATA family factors Gln3p and Nil1p, which are involved in transcriptional activation of many other nitrogen-regulated genes [4].

Biological context of GAT1

  • In agreement with this pattern of regulation, we also demonstrate the existence of Gln3p and Dal80p binding sites upstream of GAT1 [5].
  • We have selected multicopy extragenic suppressor genes, revealing that this phenotype can be suppressed by overdosing the transcription factors BDF1 and GAT1 in the yaf9Delta strain [6].
  • We have isolated the NIL1 gene, whose product is an activator of the transcription of nitrogen-regulated genes, by virtue of the homology of its zinc-finger domain to that of the previously identified activator, the product of GLN3 [3].
  • Gat1p, a GATA family protein whose production is sensitive to nitrogen catabolite repression, participates in transcriptional activation of nitrogen-catabolic genes in Saccharomyces cerevisiae [5].
  • Here we demonstrate that another positive regulator, designated Gat1p, participates in the transcription of NCR-sensitive genes and is able to weakly activate transcription when tethered upstream of a reporter gene devoid of upstream activation sequence elements [5].

Anatomical context of GAT1


Associations of GAT1 with chemical compounds

  • In the present work we showed that invertase levels displayed by the single nil1 and gln3 and by the double gln3nil1 mutant cells, cultivated in a sucrose-ammonium medium and collected at the exponential phase, were 6-, 10- and 60-fold higher, respectively, in comparison to their wild-type counterparts [9].
  • NCR, normally observed with ammonia or glutamine, is severely diminished when Gat1p is overproduced, and this inhibition is overcome by simultaneously increasing URE2 expression [10].
  • Arg82p and Kcs1p are required for activation of NCR-regulated genes in response to nitrogen availability, mainly through Nil1p, and for repression of PHO genes by phosphate [11].
  • This gene is not expressed in media containing glutamine, and its transcription is activated in response to Gln3p in cells using glutamate as the source of nitrogen and by Nil1p in cells using urea as the source of nitrogen [12].
  • Dal82p binds to the UIS(ALL) sites of allophanate-induced genes of the allantoin-degradative pathway and functions synergistically with the GATA family Gln3p and Gat1p transcriptional activators that are responsible for nitrogen catabolite repression-sensitive gene expression [13].

Physical interactions of GAT1

  • Ure2p binds to Gln3p and Gat1p and is required for NCR-sensitive transcription to be repressed and for nuclear exclusion of these transcription factors [14].
  • Ada1/Gan1p thus represents the first reported case of an accessory protein (a co-activator) linking the GATA-binding proteins Gln3p and Nil1p, mediating nitrogen-regulated transcription, to the basal transcription machinery [15].
  • This complex formation correlates with Gln3 being sequestered in the cytoplasm under conditions of excess nitrogen, where Gln3/Gat1-mediated transcription is minimal [16].

Enzymatic interactions of GAT1

  • When carbon and nitrogen are abundant, the phosphorylated Ure2p anchors the also phosphorylated Gln3p and Nil1p in the cytoplasm [9].

Regulatory relationships of GAT1

  • We show that NCR-sensitive DAL80 transcription can be influenced by the relative levels of GAT1 and URE2 expression [10].
  • Enhanced green fluorescent protein-Gat1p is nuclear when Gat1p-dependent transcription is high and cytoplasmic when it is inhibited by overproduction of Ure2p [10].

Other interactions of GAT1

  • Expression of GAT1 is shown to be NCR sensitive, partially Gln3p dependent, and Dal80p regulated [5].
  • In addition to the GATA sequences situated upstream of all nitrogen catabolite repression-sensitive genes that encode enzyme and transport proteins, the promoters of the GAT1, DAL80, and DEH1 genes all contain multiple GATA sequences as well [17].
  • Gln3p and Nil1p regulation of invertase activity and SUC2 expression in Saccharomyces cerevisiae [9].
  • We found that Nil1p and Put3p, but not Gln3p, play major roles in rapamycin-induced PUT1 expression [18].
  • Gln3p binds to and Gat1p is proposed to bind to single GATA sequences; Dal80p binds to pairs of specifically oriented and spaced GATA sequences, and Dal82p binds to a pathway-specific element, UIS(ALL) [19].
  • The paucity of analogous information concerning Gat1 regulation prompted us to investigate the effects of deleting SIT4 and URE2 on Gat1-Myc(13) localization, DNA binding, and NCR-sensitive transcription [20].


  1. Dissecting glucose signalling with diversity-oriented synthesis and small-molecule microarrays. Kuruvilla, F.G., Shamji, A.F., Sternson, S.M., Hergenrother, P.J., Schreiber, S.L. Nature (2002) [Pubmed]
  2. Carbon- and nitrogen-quality signaling to translation are mediated by distinct GATA-type transcription factors. Kuruvilla, F.G., Shamji, A.F., Schreiber, S.L. Proc. Natl. Acad. Sci. U.S.A. (2001) [Pubmed]
  3. Role of the GATA factors Gln3p and Nil1p of Saccharomyces cerevisiae in the expression of nitrogen-regulated genes. Stanbrough, M., Rowen, D.W., Magasanik, B. Proc. Natl. Acad. Sci. U.S.A. (1995) [Pubmed]
  4. A family of ammonium transporters in Saccharomyces cerevisiae. Marini, A.M., Soussi-Boudekou, S., Vissers, S., Andre, B. Mol. Cell. Biol. (1997) [Pubmed]
  5. Gat1p, a GATA family protein whose production is sensitive to nitrogen catabolite repression, participates in transcriptional activation of nitrogen-catabolic genes in Saccharomyces cerevisiae. Coffman, J.A., Rai, R., Cunningham, T., Svetlov, V., Cooper, T.G. Mol. Cell. Biol. (1996) [Pubmed]
  6. The bromodomain-containing protein Bdf1p acts as a phenotypic and transcriptional multicopy suppressor of YAF9 deletion in yeast. Bianchi, M.M., Costanzo, G., Chelstowska, A., Grabowska, D., Mazzoni, C., Piccinni, E., Cavalli, A., Ciceroni, F., Rytka, J., Slonimski, P.P., Frontali, L., Negri, R. Mol. Microbiol. (2004) [Pubmed]
  7. AtGAT1, a high affinity transporter for gamma-aminobutyric acid in Arabidopsis thaliana. Meyer, A., Eskandari, S., Grallath, S., Rentsch, D. J. Biol. Chem. (2006) [Pubmed]
  8. The GABA transporter GAT1 and the MAGUK protein Pals1: interaction, uptake modulation, and coexpression in the brain. McHugh, E.M., Zhu, W., Milgram, S., Mager, S. Mol. Cell. Neurosci. (2004) [Pubmed]
  9. Gln3p and Nil1p regulation of invertase activity and SUC2 expression in Saccharomyces cerevisiae. Oliveira, E.M., Mansure, J.J., Bon, E.P. FEMS Yeast Res. (2005) [Pubmed]
  10. Nitrogen catabolite repression of DAL80 expression depends on the relative levels of Gat1p and Ure2p production in Saccharomyces cerevisiae. Cunningham, T.S., Andhare, R., Cooper, T.G. J. Biol. Chem. (2000) [Pubmed]
  11. Arg82p is a bifunctional protein whose inositol polyphosphate kinase activity is essential for nitrogen and PHO gene expression but not for Mcm1p chaperoning in yeast. El Alami, M., Messenguy, F., Scherens, B., Dubois, E. Mol. Microbiol. (2003) [Pubmed]
  12. Two transcription factors, Gln3p and Nil1p, use the same GATAAG sites to activate the expression of GAP1 of Saccharomyces cerevisiae. Stanbrough, M., Magasanik, B. J. Bacteriol. (1996) [Pubmed]
  13. Synergistic operation of the CAR2 (Ornithine transaminase) promoter elements in Saccharomyces cerevisiae. Park, H.D., Scott, S., Rai, R., Dorrington, R., Cooper, T.G. J. Bacteriol. (1999) [Pubmed]
  14. Gln3p nuclear localization and interaction with Ure2p in Saccharomyces cerevisiae. Kulkarni, A.A., Abul-Hamd, A.T., Rai, R., El Berry, H., Cooper, T.G. J. Biol. Chem. (2001) [Pubmed]
  15. A co-activator of nitrogen-regulated transcription in Saccharomyces cerevisiae. Soussi-Boudekou, S., André, B. Mol. Microbiol. (1999) [Pubmed]
  16. In vivo specificity of Ure2 protection from heavy metal ion and oxidative cellular damage in Saccharomyces cerevisiae. Rai, R., Cooper, T.G. Yeast (2005) [Pubmed]
  17. The level of DAL80 expression down-regulates GATA factor-mediated transcription in Saccharomyces cerevisiae. Cunningham, T.S., Rai, R., Cooper, T.G. J. Bacteriol. (2000) [Pubmed]
  18. Rapamycin treatment results in GATA factor-independent hyperphosphorylation of the proline utilization pathway activator in Saccharomyces cerevisiae. Saxena, D., Kannan, K.B., Brandriss, M.C. Eukaryotic Cell (2003) [Pubmed]
  19. Roles of the Dal82p domains in allophanate/oxalurate-dependent gene expression in Saccharomyces cerevisiae. Scott, S., Abul-Hamd, A.T., Cooper, T.G. J. Biol. Chem. (2000) [Pubmed]
  20. Tor pathway control of the nitrogen-responsive DAL5 gene bifurcates at the level of Gln3 and Gat1 regulation in Saccharomyces cerevisiae. Georis, I., Tate, J.J., Cooper, T.G., Dubois, E. J. Biol. Chem. (2008) [Pubmed]
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