Journal
SCIENCE
Volume 345, Issue 6198, Pages 785-+Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1255903
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Funding
- U.K. Medical Research Council
- Wellcome Trust
- European Commission FP7, EpiGeneSys
- European Commission FP7, EpiHealth
- Pediatric Endocrine Society
- Eunice Kennedy Shriver National Institute of Child Health and Human Development, NIH
- American Diabetes Association
- Graetz Foundation
- NIH [P30DK036836]
- Novartis Research Foundation
- BBSRC [BBS/E/B/0000S266, BBS/E/B/000C0402] Funding Source: UKRI
- MRC [MR/J001597/1] Funding Source: UKRI
- Grants-in-Aid for Scientific Research [25713040] Funding Source: KAKEN
- Biotechnology and Biological Sciences Research Council [BBS/E/B/000C0402, BBS/E/B/0000S266] Funding Source: researchfish
- Medical Research Council [MR/J001597/1] Funding Source: researchfish
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Adverse prenatal environments can promote metabolic disease in offspring and subsequent generations. Animal models and epidemiological data implicate epigenetic inheritance, but the mechanisms remain unknown. In an intergenerational developmental programming model affecting F-2 mouse metabolism, we demonstrate that the in utero nutritional environment of F-1 embryos alters the germline DNA methylome of F-1 adult males in a locus-specific manner. Differentially methylated regions are hypomethylated and enriched in nucleosome-retaining regions. A substantial fraction is resistant to early embryo methylation reprogramming, which may have an impact on F-2 development. Differential methylation is not maintained in F-2 tissues, yet locus-specific expression is perturbed. Thus, in utero nutritional exposures during critical windows of germ cell development can impact the male germline methylome, associated with metabolic disease in offspring.
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