science
Title:
Early-life nutrition modulates the epigenetic state of specific rDNA genetic variants in mice
Journal:
Science 07 Jul 2016: DOI: 10.1126/science.aaf7040
Author(s):
Holland ML1, Lowe R2, Caton PW3, Gemma C2, Carbajosa G2, Danson AF2, Carpenter AA4, Loche E4, Ozanne SE4, Rakyan VK1
Author(s) affiliation:
1The Blizard Institute, Barts, and The London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK. This email address is being protected from spambots. You need JavaScript enabled to view it. This email address is being protected from spambots. You need JavaScript enabled to view it..
2The Blizard Institute, Barts, and The London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK.
3Division of Diabetes and Nutritional Sciences, King's College London, 150 Stamford Street, London SE1 9NH, UK.
4University of Cambridge Metabolic Research Laboratories and MRC Metabolic Diseases Unit, Institute of Metabolic Science, Addenbrookes Hospital, Cambridge, CB2 0QQ, UK.
 

 

Short description:
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.

Copyright © 2016, American Association for the Advancement of Science.
Link to the journal
 

 

Abstract taken from PubMed

Abstract:
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.

Copyright © 2016, American Association for the Advancement of Science.
Link to the paper on PubMed
 




 

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