期刊
EPIGENETICS
卷 7, 期 10, 页码 1200-1210出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/epi.22141
关键词
DNA methylation; genomic imprinting; differentially methylated region; developmental programming; metabolism; nutrition
资金
- Biotechnology and Biological Sciences Research Council
- Medical Research Council of the United Kingdom
- European Union
- British Heart Foundation
- Biotechnology and Biological Sciences Research Council [B/E002161/1]
- Biotechnology and Biological Sciences Research Council [BBS/E/B/0000C169, BB/D007909/1] Funding Source: researchfish
- British Heart Foundation [FS/09/029/27902] Funding Source: researchfish
- Medical Research Council [G0600717B] Funding Source: researchfish
- BBSRC [BB/D007909/1] Funding Source: UKRI
The nutritional environment in which the mammalian fetus or infant develops is recognized as influencing the risk of chronic diseases, such as type 2 diabetes and hypertension, in a phenomenon that has become known as developmental programming. The late onset of such diseases in response to earlier transient experiences has led to the suggestion that developmental programming may have an epigenetic component, because epigenetic marks such as DNA methylation or histone tail modifications could provide a persistent memory of earlier nutritional states. One class of genes that has been considered a potential target or mediator of programming events is imprinted genes, because these genes critically depend upon epigenetic modifications for correct expression and because many imprinted genes have roles in controlling fetal growth as well as neonatal and adult metabolism. In this study, we have used an established model of developmental programming-isocaloric protein restriction to female mice during gestation or lactation-to examine whether there are effects on expression and DNA methylation of imprinted genes in the offspring. We find that although expression of some imprinted genes in liver of offspring is robustly and sustainably changed, methylation of the differentially methylated regions (DMRs) that control their monoallelic expression remains largely unaltered. We conclude that deregulation of imprinting through a general effect on DMR methylation is unlikely to be a common factor in developmental programming.
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