Epigenome environment interactions accelerate epigenomic aging and unlock metabolically restricted epigenetic reprogramming in adulthood

Lindsey S. Treviño, Jianrong Dong, Ahkilesh Kaushal, Tiffany A. Katz, Rahul Kumar Jangid, Matthew J. Robertson, Sandra L. Grimm, Chandra Shekar R. Ambati, Vasanta Putluri, Aaron R. Cox, Kang Ho Kim, Thaddeus D. May, Morgan R. Gallo, David D. Moore, Sean M. Hartig, Charles E. Foulds, Nagireddy Putluri, Cristian Coarfa () and Cheryl Lyn Walker ()
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Lindsey S. Treviño: Baylor College of Medicine
Jianrong Dong: Baylor College of Medicine
Ahkilesh Kaushal: Baylor College of Medicine
Tiffany A. Katz: Baylor College of Medicine
Rahul Kumar Jangid: Baylor College of Medicine
Matthew J. Robertson: Baylor College of Medicine
Sandra L. Grimm: Baylor College of Medicine
Chandra Shekar R. Ambati: Baylor College of Medicine
Vasanta Putluri: Baylor College of Medicine
Aaron R. Cox: Baylor College of Medicine
Kang Ho Kim: Baylor College of Medicine
Thaddeus D. May: Baylor College of Medicine
Morgan R. Gallo: Baylor College of Medicine
David D. Moore: Baylor College of Medicine
Sean M. Hartig: Baylor College of Medicine
Charles E. Foulds: Baylor College of Medicine
Nagireddy Putluri: Baylor College of Medicine
Cristian Coarfa: Baylor College of Medicine
Cheryl Lyn Walker: Baylor College of Medicine

Nature Communications, 2020, vol. 11, issue 1, 1-14

Abstract: Abstract Our early-life environment has a profound influence on developing organs that impacts metabolic function and determines disease susceptibility across the life-course. Using a rat model for exposure to an endocrine disrupting chemical (EDC), we show that early-life chemical exposure causes metabolic dysfunction in adulthood and reprograms histone marks in the developing liver to accelerate acquisition of an adult epigenomic signature. This epigenomic reprogramming persists long after the initial exposure, but many reprogrammed genes remain transcriptionally silent with their impact on metabolism not revealed until a later life exposure to a Western-style diet. Diet-dependent metabolic disruption was largely driven by reprogramming of the Early Growth Response 1 (EGR1) transcriptome and production of metabolites in pathways linked to cholesterol, lipid and one-carbon metabolism. These findings demonstrate the importance of epigenome:environment interactions, which early in life accelerate epigenomic aging, and later in adulthood unlock metabolically restricted epigenetic reprogramming to drive metabolic dysfunction.

Date: 2020
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DOI: 10.1038/s41467-020-15847-z

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