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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Gene Review: 

GSR 1  -  glutamine synthetase 1;1

Arabidopsis thaliana

Synonyms: ARABIDOPSIS GLUTAMINE SYNTHASE 1;1, ARABIDOPSIS THALIANA GLUTAMINE SYNTHASE CLONE R1, ATGLN1;1, ATGSR1, GLN1;1, ...
 
 
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High impact information on ATGSR1

  • GLN1;4 was another high affinity-type GS1 expressed in nitrogen-starved plants but was 10-fold less abundant than GLN1;1 [1].
  • By contrast, the high affinity isoenzyme, GLN1;1 (Km for ammonium < 10 microm; Km for glutamate = 1.1 +/- 0.4 mm) was abundantly accumulated in the surface layers of roots during nitrogen limitation and was down-regulated by ammonium excess [1].
  • Phosphorylation assays revealed that AtGLN1;1 could be specifically phosphorylated by AtCRK3 in vitro [2].
  • In addition, both AtGLN1;1 and AtCRK3 could be induced by natural or artificially induced leaf senescence, implying that such interaction may be involved in the regulation of nitrogen remobilization during leaf senescence [2].
  • Further analyses indicated that AtGLN1;1 could interact specifically with AtCRK3 and the kinase domain of AtCRK3 and the catalytic domain of AtGLN1;1 were responsible for such interaction, respectively [2].
 

Other interactions of ATGSR1

  • Four distinct GS cDNA clones, lambda Atgsl1, lambda Atgsr1, lambda Atgsr2 and lambda Atkb6 were isolated and characterized [3].

References

  1. Kinetic properties and ammonium-dependent regulation of cytosolic isoenzymes of glutamine synthetase in Arabidopsis. Ishiyama, K., Inoue, E., Watanabe-Takahashi, A., Obara, M., Yamaya, T., Takahashi, H. J. Biol. Chem. (2004) [Pubmed]
  2. Arabidopsis cytosolic glutamine synthetase AtGLN1;1 is a potential substrate of AtCRK3 involved in leaf senescence. Li, R.J., Hua, W., Lu, Y.T. Biochem. Biophys. Res. Commun. (2006) [Pubmed]
  3. The glutamine synthetase gene family of Arabidopsis thaliana: light-regulation and differential expression in leaves, roots and seeds. Peterman, T.K., Goodman, H.M. Mol. Gen. Genet. (1991) [Pubmed]
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