Environmental epigenetics: prospects for studying epigenetic mediation of exposure-response relationships

Victoria K Cortessis, Duncan C Thomas, A Joan Levine, Carrie V Breton, Thomas M Mack, Kimberly D Siegmund, Robert W Haile, Peter W Laird, Victoria K Cortessis, Duncan C Thomas, A Joan Levine, Carrie V Breton, Thomas M Mack, Kimberly D Siegmund, Robert W Haile, Peter W Laird

Abstract

Changes in epigenetic marks such as DNA methylation and histone acetylation are associated with a broad range of disease traits, including cancer, asthma, metabolic disorders, and various reproductive conditions. It seems plausible that changes in epigenetic state may be induced by environmental exposures such as malnutrition, tobacco smoke, air pollutants, metals, organic chemicals, other sources of oxidative stress, and the microbiome, particularly if the exposure occurs during key periods of development. Thus, epigenetic changes could represent an important pathway by which environmental factors influence disease risks, both within individuals and across generations. We discuss some of the challenges in studying epigenetic mediation of pathogenesis and describe some unique opportunities for exploring these phenomena.

Figures

Fig. 1
Fig. 1
Reprogramming of DNA methylation in the zygote, early embryo, and primordial germ cells. Thickness of theouter arrows indicates levels of DNA methylation. Red maternal genome, blue paternal genome, black diploid genome. Embryonic lineages arise from cells of the inner cell mass (ICM), the placenta and extraembryonic membranes from trophectoderm cells, and the germ cell lineage from primordial germ cells following their determination from proximal epiblast. Inner circles indicate developmental stages when key elements of epigenetic programming are thought to occur (Adapted from Feng et al. 2010)
Fig. 2
Fig. 2
Schematic representation of the model for transgenerational effects

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