Journal
SCIENCE
Volume 353, Issue 6298, Pages 495-498Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aaf7040
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Funding
- Biotechnology and Biological Sciences Research Council, UK [BB/M012494/1, BB/G00711/X/1]
- Research Council UK Academic Fellowship
- EU-FP7 BLUEPRINT
- British Heart Foundation [FS/12/64/30001]
- Medical Research Council [MC_UU_12012/4]
- Queen Mary University of London Research-IT
- Engineering and Physical Sciences Research Council [EP/K000128/1]
- Biotechnology and Biological Sciences Research Council [BB/G00711X/1] Funding Source: researchfish
- British Heart Foundation [FS/09/029/27902] Funding Source: researchfish
- Medical Research Council [1649609, MC_UU_12012/4] Funding Source: researchfish
- BBSRC [BB/G00711X/1] Funding Source: UKRI
- MRC [MC_UU_12012/4] Funding Source: UKRI
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A suboptimal early-life environment, due to poor nutrition or stress during pregnancy, can influence lifelong phenotypes in the progeny. Epigenetic factors are thought to be key mediators of these effects. We show that protein restriction in mice from conception until weaning induces a linear correlation between growth restriction and DNA methylation at ribosomal DNA (rDNA). This epigenetic response remains into adulthood and is restricted to rDNA copies associated with a specific genetic variant within the promoter. Related effects are also found in models of maternal high-fat or obesogenic diets. Our work identifies environmentally induced epigenetic dynamics that are dependent on underlying genetic variation and establishes rDNA as a genomic target of nutritional insults.
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