TY  - JOUR
AU  - Sato, Noriko
AU  - Kubota, Takeo
AU  - Imai, Chihiro
AU  - Mochizuki, Kazuki
PY  - 2017
DA  - 2017/10/19
TI  - The Role of Epigenetics in Developmental Programming and the Developmental Origins of Health and Disease
JO  - OBM Genetics
SP  - 008
VL  - 01
IS  - 04
AB  - A number of epidemiological studies have suggested that environmental stresses, such as malnutrition during the fetal period, can induce development of metabolic disorders, such as obesity, type 2 diabetes and hypertension, and psychiatric disorders in later life. This theory is known as the Developmental Origins of Health and Disease (DOHaD), in which “epigenetic memories”, involving DNA methylation, histone modifications and microRNA expression, are induced by environmental stresses during development. For example, the binding of transcription factors to cis-elements within the promoters and enhancer regions of genes induces demethylation and subsequent histone acetylation and transcriptional activation. Several lines of evidence suggest that binding of bromodomain-containing protein 4 and positive transcription elongation factor B to acetylated histones within “gene body” regions initiates transcriptional elongation and, inversely, histone H3K36 methylation and DNA methylation within “gene body” regions terminates this transcriptional elongation. This new epigenetic model of the gene body can be applied to the regulation of metabolic genes, which respond to carbohydrate signals and are associated with energy balance. Recent studies indicate that these new gene body epigenetic mechanisms, as well as the classical promoter/enhancer mechanism, are involved in epigenetic changes found in offspring that have been exposed to malnutrition during the fetal period. In this context, further understanding of epigenetic gene regulation based on the “gene body epigenetic model” will provide new preventive and therapeutic strategies for adult diseases encompassed by DOHaD theory.
SN  - 2577-5790
UR  - https://doi.org/10.21926/obm.genet.1704008
DO  - 10.21926/obm.genet.1704008
ID  - Sato2017
ER  -