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Sculpting Our Future: Environmental Nudging of the Imprintome

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Environmental Epigenomics in Health and Disease

Part of the book series: Epigenetics and Human Health ((EHH))

Abstract

Over the past several decades, there has been a dramatic increase in awareness of the importance of epigenetics in the regulation of gene expression and how this relates to disease. The initial focus on cancer as a potential outcome of epigenetic alterations has grown to include the role of epigenetics in neurodevelopmental disorders, obesity, diabetes, memory, and even deviation in complex human social interactions. Prominent among the genes implicated in all of these conditions are those subject to genomic imprinting. These genes are regulated by epigenetic mechanisms, including DNA methylation that is established during early development and results in parent of origin dependent expression. Advances in the ability to accurately measure DNA methylation using high throughput techniques have now paved the way for study of this epigenetic modification in epidemiologic studies. In this chapter, we will examine the relationship of the early origins hypothesis to imprinted genes and how emerging studies strongly suggest that early origins may in part have its roots in epigenetic changes at these imprinted regulatory regions during early life.

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Abbreviations

BWS:

Beckwith Wiedemann Syndrome

CDKN1C:

Cyclin-Dependent Kinase Inhibitor 1C

CTCF:

CCCTC Binding Factor

DLK1:

Delta Like 1 Homolog (Drosophila)

DMR:

Differentially Methylated Region

DNMT:

DNA Methyltransferase

GNAS:

Guanine Nucleotide Binding Protein (G protein) Alpha Stimulating Activity Polypeptide

GRB10:

Growth Factor Receptor-Bound Protein 10

H19:

Maternally Expressed H19

HYMAI:

Hydatidiform Mole Associated and Imprinted (Non-Protein Coding)

IGF1R:

Insulin-like Growth Factor Type I Receptor

IGF2:

Insulin-like Growth Factor II

KCNQ1OT1 KCNQ1:

Opposite Strand/Antisense Transcript (Non-Protein Coding)

MEG3:

Maternally Expressed Gene 3 (Non-Protein Coding)

MEST:

Mesoderm Specific Transcript Homolog (Mouse)

NDN:

Necdin

NEST:

Newborn Epigenetics STudy

NNAT:

Neuronatin

PLAGL1:

Pleomorphic Adenoma Gene-Like 1

PEG3:

Paternally Expressed Gene 3

SGCE:

Epsilon Sarcoglycan

SLC38A4:

Solute Carrier Family 38 Member 4

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Acknowledgments

We thank the participants of the Newborn Epigenetics STudy and gratefully acknowledge the NEST support staff for their hard work and dedication to the project. This research was supported by National Institutes of Health grants R21ES014947, R01ES016772, and R01DK085173 and by funding from the Duke Comprehensive Cancer Center.

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Authors and Affiliations

  1. Department of Obstetrics and Gynecology, Duke University Medical Center, Room B226 LSRC, 91012, Durham, NC, 27708, USA

    Susan K. Murphy

  2. Department of Obstetrics and Gynecology, Duke University Medical Center, Durham, NC, 27710, USA

    Cathrine Hoyo

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  1. Susan K. Murphy
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  2. Cathrine Hoyo
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Correspondence to Susan K. Murphy .

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Editors and Affiliations

  1. School of Medicine and Public Health, McArdle Laboratory for Cancer Research, University of Wisconsin-Madison, University Avenue 1400, Madison, 53706, Wisconsin, USA

    Randy L Jirtle

  2. National Institute of Environmental Hea, NIEHS, National Institutes of Health, Research Triangle Park, 27709, North Carolina, USA

    Frederick L. Tyson

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Murphy, S.K., Hoyo, C. (2013). Sculpting Our Future: Environmental Nudging of the Imprintome. In: Jirtle, R., Tyson, F. (eds) Environmental Epigenomics in Health and Disease. Epigenetics and Human Health. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-23380-7_3

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