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Gene Review:

DME - transcriptional activator DEMETER

Arabidopsis thaliana

Synonyms: AT5G04570, AT5G04580, DEMETER, T32M21.160, T32M21_160

Choi, Y. et al., Morales-Ruiz, T. et al., Gehring, M. et al., Xiao, W. et al., Choi, Y. et al., et al.

Kinoshita, Miura, Choi, Kinoshita, Cao, Jacobsen, Fischer, Kakutani,

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Disease relevance of DME

DME can excise 5-methylcytosine in vitro and when expressed in E. coli [1].

High impact information on DME

Thus, DME establishes MEA imprinting by removing 5-methylcytosine to activate the maternal allele [1].
Abasic sites opposite 5-methylcytosine inhibit DME activity and might prevent DME from generating double-stranded DNA breaks [1].
DEMETER, a DNA glycosylase domain protein, is required for endosperm gene imprinting and seed viability in arabidopsis [2].
In Arabidopsis thaliana, DEMETER (DME) activates the maternal expression of two imprinted genes silenced by methylation, and REPRESSOR OF SILENCING 1 (ROS1) is required for release of transcriptional silencing of a hypermethylated transgene [3].
Transgenes expressing wild-type DME in the central cell rescue seed abortion caused by a mutation in the endogenous DME gene and activate maternal MEA:GFP transcription [4].

Biological context of DME

However, transgenes expressing the D1304N mutant DME do not rescue seed abortion or activate maternal MEA:GFP transcription [4].
These results show that the conserved aspartic acid residue is necessary for DME to function in vivo and suggest that an active DNA glycosylase domain, normally associated with DNA repair, promotes gene transcription that is essential for gene imprinting [4].
An invariant aspartic acid in the DNA glycosylase domain of DEMETER is necessary for transcriptional activation of the imprinted MEDEA gene [4].
It is established by maternal gametophyte-specific gene activation, which depends on a DNA glycosylase gene, DEMETER [5].

Regulatory relationships of DME

Ectopic DME expression in endosperm activates expression of the normally silenced paternal MEA allele [2].
DME activates whereas MET1 suppresses maternal MEA::GFP allele expression in the central cell [6].

Other interactions of DME

These findings suggest that a function of ROS1 and DME is to initiate erasure of 5-meC through a base excision repair process and provide strong biochemical evidence for the existence of an active DNA demethylation pathway in plants [3].
Our data suggest that imprinting is controlled in the female gametophyte by antagonism between the two DNA-modifying enzymes, MET1 methyltransferase and DME DNA glycosylase [6].

References

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]
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]
DEMETER and REPRESSOR OF SILENCING 1 encode 5-methylcytosine DNA glycosylases. Morales-Ruiz, T., Ortega-Galisteo, A.P., Ponferrada-Marín, M.I., Martínez-Macías, M.I., Ariza, R.R., Roldán-Arjona, T. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
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]
One-way control of FWA imprinting in Arabidopsis endosperm by DNA methylation. Kinoshita, T., Miura, A., Choi, Y., Kinoshita, Y., Cao, X., Jacobsen, S.E., Fischer, R.L., Kakutani, T. Science (2004) [Pubmed]
Imprinting of the MEA Polycomb gene is controlled by antagonism between MET1 methyltransferase and DME glycosylase. Xiao, W., Gehring, M., Choi, Y., Margossian, L., Pu, H., Harada, J.J., Goldberg, R.B., Pennell, R.I., Fischer, R.L. Dev. Cell (2003) [Pubmed]

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