Neonatal thyroxine activation modifies epigenetic programming of the liver

Tatiana L. Fonseca, Tzintzuni Garcia, Gustavo W. Fernandes, T. Murlidharan Nair and Antonio C. Bianco ()
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Tatiana L. Fonseca: University of Chicago
Tzintzuni Garcia: University of Chicago
Gustavo W. Fernandes: University of Chicago
T. Murlidharan Nair: Indiana University South Bend
Antonio C. Bianco: University of Chicago

Nature Communications, 2021, vol. 12, issue 1, 1-11

Abstract: Abstract The type 2 deiodinase (D2) in the neonatal liver accelerates local thyroid hormone triiodothyronine (T3) production and expression of T3-responsive genes. Here we show that this surge in T3 permanently modifies hepatic gene expression. Liver-specific Dio2 inactivation (Alb-D2KO) transiently increases H3K9me3 levels during post-natal days 1–5 (P1–P5), and results in methylation of 1,508 DNA sites (H-sites) in the adult mouse liver. These sites are associated with 1,551 areas of reduced chromatin accessibility (RCA) within core promoters and 2,426 within intergenic regions, with reduction in the expression of 1,363 genes. There is strong spatial correlation between density of H-sites and RCA sites. Chromosome conformation capture (Hi-C) data reveals a set of 81 repressed genes with a promoter RCA in contact with an intergenic RCA ~300 Kbp apart, within the same topologically associating domain (χ2 = 777; p

Date: 2021
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DOI: 10.1038/s41467-021-24748-8

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