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'Hot off the press' is a daily listing of the most recent articles in epigenetics and imprinting

Environmental Epigenomics in Health and Disease

22 July 2013: Springer has recently published two books on environmental epigenomics that are edited by Randy L. Jirtle and Frederick L. Tyson -- Epigenetics and Disease Origins and Epigenetics and Complex Diseases. The overall purpose of these books is to give readers an overview of how environmental exposures can influence the risk of disease in adulthood by disrupting epigenetic processes and reprogramming during early development. Leading investigators in the field of epigenetics discuss patterns of epigenomic modifications in normal cells, and how environmentally-induced changes in them are associated with disease pathogenesis. The authors comprehensively review epigenetic processes that occur in human embryonic stem cells, as well as in differentiating cells and organs such as the brain, and discuss autism, schizophrenia, and sexual dimorphism in the developing brains of males and females. Legal and ethical implications of such epigenetic alterations are also assessed. These books represent our attempt to bring the field of environmental epigenomics to a rapidly growing audience.

Radiation Epigenetics

Humans are exposed to low-dose ionizing radiation (LDIR) from a number of environmental and medical sources. In addition to inducing genetic mutations, there is concern that LDIR may also alter the epigenome. Such heritable effects early in life can either be positively adaptive or result in the enhanced formation of diseases, including cancer, diabetes, and obesity. In this study, we show that LDIR significantly increases DNA methylation at the viable yellow agouti (Avy) locus in a dose- and sex-dependent manner. Moreover, maternal dietary antioxidant supplementation mitigated both the DNA methylation changes and coat color shift in the irradiated offspring. Thus, LDIR exposure during gestation elicits epigenetic alterations that lead to positive adaptive phenotypic changes that are negated with antioxidants, indicating they are mediated in part by oxidative stress. Read more...

These Little Piggies!

Imprinted genes are monnoallelically expressed in a parent-of-origin dependent manner because the same parental allele is always epigenetically silenced (Jirtle and Weidman 2007). The phenomenon of genomic imprinting evolved in mammals around 200 million years ago in a common ancestor to marsupials and eutherians (Killian et al. 2000). Once this unique epigenetic form of gene regulation evolved, natural selection may have utilized the resulting marked variation in gene expression to drive mammalian speciation, providing a plausible explanation for why mammalian species vary markedly in their imprinted gene repertoires. Read more...

Epigenetic Basis of Suicide Risk?

Not all multigenerational effects are transmitted through the germ line. Elegant studies in rats demonstrate that generation-to-generation attainment of the nurturing behaviors of pup licking and grooming and arch-back nursing are not germline inherited. Rather, they are passed on to the offspring directly from the mother during the first week of postnatal life through the induction of DNA methylation and histone alterations in the hippocampus (Weaver et al. 2004). Moreover, the inherent plasticity of the epigenome allows for the reversal of these modifications in adulthood by exposure to epigenetic therapeutic agents (Weaver et al. 2006). Read more...

Genome-wide Mapping of Human Imprinted Genes

Genomic imprinting is an epigenetic form of gene regulation that results in only the copy inherited from the mother or father to function. (Jirtle and Weidman 2007). The phenomenon of imprinting evolved about 150 M years ago in a common ancester to mammals that have live birth - the Therian mammals (Marsupials and Eutherians) (Killian et al. 2000). Read more...

Negative Bisphenol A Effects on the Epigenome Blocked by Nutritional Supplements

The hypothesis of fetal origins of adult disease proposes that early developmental exposures involve epigenetic modifications, such as DNA methylation, that influence adult disease susceptibility (Jirtle and Skinner). In utero or neonatal exposure to bisphenol A (BPA), a high-production-volume chemical used in the manufacture of polycarbonate plastic, is associated with higher body weight, increased breast and prostate cancer, and altered reproductive function (Maffini et al.). Read more...