Mouse models of epigenetic inheritance
This chapter discusses the mouse models of epigenetic inheritance. The increasing evidence implicates epigenetic changes as a primary impetus in disease development. The epigenetic regulation alters gene expression to promote compensatory adjustments in metabolism. These early adaptive epigenetic changes have consequences later in life when the metabolic changes no longer coincide with the external environment, resulting in pathologies such as coronary heart disease and obesity. The abnormal paternal epigenetic inheritance indicates that another epigenetic mark aside from DNA methylation is incompletely cleared in the heterozygous knockout offspring and leads to epigenetic inheritance and phenotypic change. Mouse models have become powerful tools for examining transgenerational inheritance of epigenetic marks as well as unique biosensors for early developmental exposures to nutritional supplements and chemical contaminants that disrupt epigenetic programming. With the increased utility of these models, our understanding of epigenetic mark inheritance at metastable epialleles and imprinted genes, and across the genome, will expand. As the model is more completely defined, the possibilities increase for their expanded use to address a broad array of research questions involved in complex human disease such as diabetes, neurological disorders, and cancer. © 2011 Elsevier Inc. All rights reserved.
Bernal, AJ; Murphy, SK; Jirtle, RL
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