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Gene Review

MEA  -  histone-lysine N-methyltransferase MEDEA

Arabidopsis thaliana

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Disease relevance of MEA

  • Sequence and deletion analysis using both transient Agrobacterium tumefaciens expression and stable transformation assays have shown that the rust-inducible fis1 promoter is contained within a 580-bp fragment [1].

High impact information on MEA

  • Thus, DME establishes MEA imprinting by removing 5-methylcytosine to activate the maternal allele [2].
  • Rather, Polycomb group proteins that are expressed from the maternal genome, including MEA, control paternal MEA silencing [2].
  • Remarkably, they also find that silencing of the paternal MEDEA allele is independent of DNA methylation and is controlled by maternal expression of MEDEA itself [3].
  • Here, we show that PHE1 is mainly paternally expressed but maternally repressed and that this maternal repression of PHE1 breaks down in seeds lacking maternal MEA activity [4].
  • MEA encodes a SET domain protein similar to Enhancer of zeste, a member of the Polycomb group [5].

Biological context of MEA


Associations of MEA with chemical compounds


Physical interactions of MEA


Regulatory relationships of MEA


Other interactions of MEA

  • The Polycomb-group (PcG) proteins MEDEA, FERTILIZATION INDEPENDENT ENDOSPERM, and FERTILIZATION INDEPENDENT SEED2 regulate seed development in Arabidopsis by controlling embryo and endosperm proliferation [6].
  • In summary, our results demonstrate that seed abortion in the medea mutant is largely mediated by deregulated expression of the type I MADS-box gene PHE1 [6].
  • By using a yeast two-hybrid screen, we identified MEA and a related protein, SWINGER (SWN), as SET-domain partners of FIS2 [12].
  • Although FIE and MEA interact, differences in maternal versus paternal patterns of expression, as well as the effect of a recessive mutation in the DECREASE IN DNA METHYLATION1 (DDM1) gene on mutant allele transmission, indicate that fie and mea mutations cause parent-of-origin effects on seed development by distinct mechanisms [13].
  • In Arabidopsis thaliana, maternal imprinting has been clearly demonstrated for the Polycomb group gene MEDEA (MEA) and for FWA [7].


  1. A plant gene up-regulated at rust infection sites. Ayliffe, M.A., Roberts, J.K., Mitchell, H.J., Zhang, R., Lawrence, G.J., Ellis, J.G., Pryor, T.J. Plant Physiol. (2002) [Pubmed]
  2. DEMETER DNA glycosylase establishes MEDEA polycomb gene self-imprinting by allele-specific demethylation. Gehring, M., Huh, J.H., Hsieh, T.F., Penterman, J., Choi, Y., Harada, J.J., Goldberg, R.B., Fischer, R.L. Cell (2006) [Pubmed]
  3. MEDEA takes control of its own imprinting. Arnaud, P., Feil, R. Cell (2006) [Pubmed]
  4. The Arabidopsis thaliana MEDEA Polycomb group protein controls expression of PHERES1 by parental imprinting. Köhler, C., Page, D.R., Gagliardini, V., Grossniklaus, U. Nat. Genet. (2005) [Pubmed]
  5. Maternal control of embryogenesis by MEDEA, a polycomb group gene in Arabidopsis. Grossniklaus, U., Vielle-Calzada, J.P., Hoeppner, M.A., Gagliano, W.B. Science (1998) [Pubmed]
  6. The Polycomb-group protein MEDEA regulates seed development by controlling expression of the MADS-box gene PHERES1. Köhler, C., Hennig, L., Spillane, C., Pien, S., Gruissem, W., Grossniklaus, U. Genes Dev. (2003) [Pubmed]
  7. Maintenance of DNA methylation during the Arabidopsis life cycle is essential for parental imprinting. Jullien, P.E., Kinoshita, T., Ohad, N., Berger, F. Plant Cell (2006) [Pubmed]
  8. Dynamic regulatory interactions of Polycomb group genes: MEDEA autoregulation is required for imprinted gene expression in Arabidopsis. Baroux, C., Gagliardini, V., Page, D.R., Grossniklaus, U. Genes Dev. (2006) [Pubmed]
  9. An invariant aspartic acid in the DNA glycosylase domain of DEMETER is necessary for transcriptional activation of the imprinted MEDEA gene. Choi, Y., Harada, J.J., Goldberg, R.B., Fischer, R.L. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  10. Arabidopsis MSI1 is a component of the MEA/FIE Polycomb group complex and required for seed development. Köhler, C., Hennig, L., Bouveret, R., Gheyselinck, J., Grossniklaus, U., Gruissem, W. EMBO J. (2003) [Pubmed]
  11. DEMETER, a DNA glycosylase domain protein, is required for endosperm gene imprinting and seed viability in arabidopsis. Choi, Y., Gehring, M., Johnson, L., Hannon, M., Harada, J.J., Goldberg, R.B., Jacobsen, S.E., Fischer, R.L. Cell (2002) [Pubmed]
  12. Partially redundant functions of two SET-domain polycomb-group proteins in controlling initiation of seed development in Arabidopsis. Wang, D., Tyson, M.D., Jackson, S.S., Yadegari, R. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  13. Mutations in the FIE and MEA genes that encode interacting polycomb proteins cause parent-of-origin effects on seed development by distinct mechanisms. Yadegari, R., Kinoshita, T., Lotan, O., Cohen, G., Katz, A., Choi, Y., Katz, A., Nakashima, K., Harada, J.J., Goldberg, R.B., Fischer, R.L., Ohad, N. Plant Cell (2000) [Pubmed]
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