Epigenetic deregulation of imprinting in congenital diseases of aberrant growth

Article Abstract:

Human chromosomes 11p15 comprises two imprinted domains, which are important in the control fetal and postnatal growth which was studied by imprinting epigenetically deregulated in Silver-Russell Syndrome (SRS), a congenital disease of growth retardation and asymmetry. It showed that fetal and postnatal growth is epigenetically controlled by different imprinting control regions (ICRs) at 11p15 and other chromosomal regions.

Health aspects, Mammals, Human chromosomes, Russell-Silver syndrome

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MEDEA takes control of its own imprinting

Article Abstract:

The activation of the maternal copy of the imprinted MEDEA Polycomb gene by DEMETER is discussed. It is demonstrated that this activation involves DNA demethylation of MEDEA by DMETER, which shows that silencing of the paternal MEDEA allele is independent of DNA methylation, and is controlled by maternal expression of MEDEA itself.

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DEMETER DNA glycosylase establishes MEDEA polycomb gene self-imprinting by allele-specific demethylation

Article Abstract:

DNA glycosylase DEMETER (DME) establishes endosperm maternal-allele-specific hypomethylation at the MEDEA (MEA) gene. DME removes 5-methylcytosine for activating the maternal allele and thus establishes MEA imprinting.

California, Usage

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