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

Antagonistic Growth Promoting Effects of Imprinted Genes

14 January 2015: Imprinted genes are monoallelic expressed in a parent-of-origin dependent manner (Jirtle and Weidman 2007).The conflict theory of genomic imprinting predicts that maternally expressed genes are antigrowth while paternally expressed genes are progrowth (Haig and Graham 1991). The first two genes experimentally identified to be imprinted, the maternally expressed Igf2r (Barlow et al. 1991) and the paternally expressed Igf2 (DeChiara et al. 1991), were shown over two decades ago to adhere to this prediction. A second set of oppositely imprinted, fetal growth antagonistic genes has now been identified, the maternally expressed Grb10 and the paternally expressed Dlk1 (Madon-Simon et al. 2014). Grb10 encodes for an intracellular signaling adaptor protein that restricts fetal growth and promotes fat deposition. In contrast, Dlk1 encodes for a ligand that promotes fetal growth and restricts fat deposition. Deregulation of DLK1 expression by a single point mutation also results in the muscle hypertrophic, callipyge (i.e. beautiful buttock) phenotype in sheep (Freking et al. 2002). Thus, there may be an evolutionary conflict between genes of maternal and paternal origin over the optimal proportions of body fat and lean muscle mass (Haig 2014).

Autism and Schizophrenia: The Antithesis of Each Other?

Genomic imprinting is a phenomenon where one parental allele is silenced epigenetically, resulting in monoallelic parent-of-origin gene expression (Jirtle and Weidman 2007). It evolved about 150 million years ago with the advent of viviparity and placentation in a common ancestor to Therian mammals (i.e. Marsupials and Eutherians) (Killian et al. 2000). Badcock and Crespi postulated in their imprinted brain theory that autism spectrum disorders (AS) and schizophrenia spectrum (SS) disorders are the antithesis of each other, and result from the skewing of paternally and maternally imprinted gene expression in the brain during development. Paternally expressed imprinted genes tend to be progrowth, and those that are maternally expressed antigrowth. Read more...

Environmental Epigenomics in Health and Disease

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. Read more...

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...