4.8 Article

Early-life nutrition modulates the epigenetic state of specific rDNA genetic variants in mice

期刊

SCIENCE
卷 353, 期 6298, 页码 495-498

出版社

AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aaf7040

关键词

-

资金

  1. Biotechnology and Biological Sciences Research Council, UK [BB/M012494/1, BB/G00711/X/1]
  2. Research Council UK Academic Fellowship
  3. EU-FP7 BLUEPRINT
  4. British Heart Foundation [FS/12/64/30001]
  5. Medical Research Council [MC_UU_12012/4]
  6. Queen Mary University of London Research-IT
  7. Engineering and Physical Sciences Research Council [EP/K000128/1]
  8. Biotechnology and Biological Sciences Research Council [BB/G00711X/1] Funding Source: researchfish
  9. British Heart Foundation [FS/09/029/27902] Funding Source: researchfish
  10. Medical Research Council [1649609, MC_UU_12012/4] Funding Source: researchfish
  11. BBSRC [BB/G00711X/1] Funding Source: UKRI
  12. MRC [MC_UU_12012/4] Funding Source: UKRI

向作者/读者索取更多资源

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.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.8
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据