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Journal ArticleDOI

Genomic imprinting: parental influence on the genome

TLDR
The study of imprinting provides new insights into epigenetic gene modification during development, and is thought to influence the transfer of nutrients to the fetus and the newborn from the mother.
Abstract
Genomic imprinting affects several dozen mammalian genes and results in the expression of those genes from only one of the two parental chromosomes. This is brought about by epigenetic instructions--imprints--that are laid down in the parental germ cells. Imprinting is a particularly important genetic mechanism in mammals, and is thought to influence the transfer of nutrients to the fetus and the newborn from the mother. Consistent with this view is the fact that imprinted genes tend to affect growth in the womb and behaviour after birth. Aberrant imprinting disturbs development and is the cause of various disease syndromes. The study of imprinting also provides new insights into epigenetic gene modification during development.

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Citations
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Journal ArticleDOI

Epigenetic regulation of gene expression: how the genome integrates intrinsic and environmental signals

TL;DR: Advances in the understanding of the mechanism and role of DNA methylation in biological processes are reviewed, showing that epigenetic mechanisms seem to allow an organism to respond to the environment through changes in gene expression.
Journal ArticleDOI

Epigenetic Reprogramming in Mammalian Development

TL;DR: What is known about reprogramming in mammals and how it might relate to developmental potency and imprinting are discussed, including whether or not methylation is involved in the control of gene expression during normal development.
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Dna methylation and human disease

TL;DR: A large number of human diseases have been found to be associated with aberrant DNA methylation and the study of these diseases has provided new and fundamental insights into the roles that DNAmethylation and other epigenetic modifications have in development and normal cellular homeostasis.
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Epigenetic Transgenerational Actions of Endocrine Disruptors and Male Fertility

TL;DR: The ability of an environmental factor to reprogram the germ line and to promote a transgenerational disease state has significant implications for evolutionary biology and disease etiology.
Journal ArticleDOI

Environmental epigenomics and disease susceptibility.

TL;DR: An increasing body of evidence from animal studies supports the role of environmental epigenetics in disease susceptibility and recent studies have demonstrated for the first time that heritable environmentally induced epigenetic modifications underlie reversible transgenerational alterations in phenotype.
References
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Journal ArticleDOI

DNA methyltransferases Dnmt3a and Dnmt3b are essential for de novo methylation and mammalian development.

TL;DR: It is demonstrated that two recently identified DNA methyltransferases, DnMT3a and Dnmt3b, are essential for de novo methylation and for mouse development and play important roles in normal development and disease.
Journal ArticleDOI

Role for DNA methylation in genomic imprinting

TL;DR: It is demonstrated that a normal level of DNA methylation is required for controlling differential expression of the paternal and maternal alleles of imprinted genes in mutant mice that are deficient in DNA methyltransferase activity.
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Methylation-induced repression--belts, braces, and chromatin.

TL;DR: Although the signals that cause susceptibility or resistance to methylation are still unknown, genetic approaches in plants are leading the way forward and exciting revelations are expected as the knowledge vacuum in this area is filled over the next few years.
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Parental imprinting of the mouse insulin-like growth factor II gene

TL;DR: It is demonstrated that IGF-II is indispensable for normal embryonic growth and that the IGF- II gene is subject to tissue-specific parental imprinting.
Journal ArticleDOI

Methylation of a CTCF-dependent boundary controls imprinted expression of the Igf2 gene

TL;DR: The results reveal that DNA methylation can control gene expression by modulating enhancer access to the gene promoter through regulation of an enhancer boundary.
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