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Ehmt2  -  euchromatic histone lysine N...

Mus musculus

Synonyms: Bat8, D17Ertd710e, Euchromatic histone-lysine N-methyltransferase 2, G9a, H3-K9-HMTase 3, ...
 
 
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Disease relevance of Ehmt2

  • Role of histone methyltransferase G9a in CpG methylation of the Prader-Willi syndrome imprinting center [1].
  • Lysine-specific murine histone H3 methyltransferase, G9a, was expressed and purified in a baculovirus expression system [2].
  • In addition to the activation of G9a, our results also indicated that hypoxia increased H3K9me2 by inhibiting H3K9 demethylation processes [3].
 

High impact information on Ehmt2

  • Histone methyltransferases G9a and GLP form heteromeric complexes and are both crucial for methylation of euchromatin at H3-K9 [4].
  • GLP-deficiency led to embryonic lethality, a severe reduction of H3-K9 mono- and dimethylation, the induction of Mage-a gene expression, and HP1 relocalization in embryonic stem cells, all of which were phenotypes of G9a-deficiency [4].
  • G9a is the major mammalian H3-K9 methyltransferase that targets euchromatic regions and is essential for murine embryogenesis [4].
  • G9a-deficient ES cells also exhibited reduced H3-K9 methylation compared to wild-type cells, indicating that G9a is a dominant H3-K9 HMTase in vivo [5].
  • Our results indicate that euchromatic H3-K9 methylation regulated by G9a is essential for early embryogenesis and is involved in the transcriptional repression of developmental genes [5].
 

Biological context of Ehmt2

 

Anatomical context of Ehmt2

  • However, analysis of this region in G9a mutant embryonic stem cells shows that these two methyl marks are dependent on different histone methyltransferases [8].
  • Co-expression of G9a and H3 resulted in di- and tri-methylation of H3-K9, while siRNA-mediated knockdown of G9a in HeLa cells resulted in reduction of global H3-K9 di- and tri-methylation [9].
 

Associations of Ehmt2 with chemical compounds

  • G9a histone methyltransferase plays a dominant role in euchromatic histone H3 lysine 9 methylation and is essential for early embryogenesis [5].
  • GST fusion proteins containing various lengths of the histone H3 amino-terminal tail were used as substrates in the presence of recombinant G9a enzyme and AdoMet cosubstrate [6].
  • A recombinant deletion mutant enzyme fused with maltose-binding protein (MBP-G9aDelta634) was used for steady-state kinetic analysis with various substrates and was compared with full-length G9a (G9aFL) [9].
  • Hypoxic mimetics, such as deferoxamine and dimethyloxalylglycine, were also found to increase H3K9me2 as well as G9a protein and activity [3].
  • To test whether HMT activity influences euchromatic cytosine methylation, we analyzed the DNA methylation status of approximately 2000 CpG-rich loci, which are predicted in silico, in G9a(-/-) embryonic stem cells by restriction landmark genomic scanning (RLGS) [10].
  • As with methylation of H3 lysine 9, autocatalytic G9a methylation is necessary and sufficient to mediate in vivo interaction with the epigenetic regulator heterochromatin protein 1 (HP1), and this methyl-dependent interaction can be reversed by adjacent G9a phosphorylation [11].
 

Other interactions of Ehmt2

  • G9a-mediated irreversible epigenetic inactivation of Oct-3/4 during early embryogenesis [12].
  • We show by RNA fluorescence in situ hybridization (FISH) that expression of Snrpn, an imprinted gene regulated by the PWS-IC, is biallelic in G9a -/- ES cells, indicating loss of imprinting [1].
  • Expression of Xist, which is crucial for the initiation of X-inactivation, was properly regulated and the inactivated X chromosome was stably maintained even in the absence of G9a [7].
  • Zinc finger protein Wiz links G9a/GLP histone methyltransferases to the co-repressor molecule CtBP [13].
  • Trimethylated peptides acted as a competitive inhibitor to substrate peptide and mixed inhibitor to AdoMet suggesting a random mechanism in a Bi Bi reaction for recombinant G9a where either substrate can bind first to the enzyme, and either product can release first [2].
 

Analytical, diagnostic and therapeutic context of Ehmt2

References

  1. Role of histone methyltransferase G9a in CpG methylation of the Prader-Willi syndrome imprinting center. Xin, Z., Tachibana, M., Guggiari, M., Heard, E., Shinkai, Y., Wagstaff, J. J. Biol. Chem. (2003) [Pubmed]
  2. Substrate specificity and kinetic mechanism of mammalian G9a histone H3 methyltransferase. Patnaik, D., Chin, H.G., Estève, P.O., Benner, J., Jacobsen, S.E., Pradhan, S. J. Biol. Chem. (2004) [Pubmed]
  3. Hypoxic Stress Induces Dimethylated Histone H3 Lysine 9 through Histone Methyltransferase G9a in Mammalian Cells. Chen, H., Yan, Y., Davidson, T.L., Shinkai, Y., Costa, M. Cancer Res. (2006) [Pubmed]
  4. Histone methyltransferases G9a and GLP form heteromeric complexes and are both crucial for methylation of euchromatin at H3-K9. Tachibana, M., Ueda, J., Fukuda, M., Takeda, N., Ohta, T., Iwanari, H., Sakihama, T., Kodama, T., Hamakubo, T., Shinkai, Y. Genes Dev. (2005) [Pubmed]
  5. G9a histone methyltransferase plays a dominant role in euchromatic histone H3 lysine 9 methylation and is essential for early embryogenesis. Tachibana, M., Sugimoto, K., Nozaki, M., Ueda, J., Ohta, T., Ohki, M., Fukuda, M., Takeda, N., Niida, H., Kato, H., Shinkai, Y. Genes Dev. (2002) [Pubmed]
  6. Sequence specificity and role of proximal amino acids of the histone H3 tail on catalysis of murine G9A lysine 9 histone H3 methyltransferase. Chin, H.G., Pradhan, M., Estève, P.O., Patnaik, D., Evans, T.C., Pradhan, S. Biochemistry (2005) [Pubmed]
  7. X-inactivation is stably maintained in mouse embryos deficient for histone methyl transferase G9a. Ohhata, T., Tachibana, M., Tada, M., Tada, T., Sasaki, H., Shinkai, Y., Sado, T. Genesis (2004) [Pubmed]
  8. Differential histone H3 Lys-9 and Lys-27 methylation profiles on the X chromosome. Rougeulle, C., Chaumeil, J., Sarma, K., Allis, C.D., Reinberg, D., Avner, P., Heard, E. Mol. Cell. Biol. (2004) [Pubmed]
  9. Functional analysis of the N- and C-terminus of mammalian G9a histone H3 methyltransferase. Estève, P.O., Patnaik, D., Chin, H.G., Benner, J., Teitell, M.A., Pradhan, S. Nucleic Acids Res. (2005) [Pubmed]
  10. Genome-wide and locus-specific DNA hypomethylation in G9a deficient mouse embryonic stem cells. Ikegami, K., Iwatani, M., Suzuki, M., Tachibana, M., Shinkai, Y., Tanaka, S., Greally, J.M., Yagi, S., Hattori, N., Shiota, K. Genes Cells (2007) [Pubmed]
  11. Methylation of a histone mimic within the histone methyltransferase G9a regulates protein complex assembly. Sampath, S.C., Marazzi, I., Yap, K.L., Sampath, S.C., Krutchinsky, A.N., Mecklenbräuker, I., Viale, A., Rudensky, E., Zhou, M.M., Chait, B.T., Tarakhovsky, A. Mol. Cell (2007) [Pubmed]
  12. G9a-mediated irreversible epigenetic inactivation of Oct-3/4 during early embryogenesis. Feldman, N., Gerson, A., Fang, J., Li, E., Zhang, Y., Shinkai, Y., Cedar, H., Bergman, Y. Nat. Cell Biol. (2006) [Pubmed]
  13. Zinc finger protein Wiz links G9a/GLP histone methyltransferases to the co-repressor molecule CtBP. Ueda, J., Tachibana, M., Ikura, T., Shinkai, Y. J. Biol. Chem. (2006) [Pubmed]
 
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