Epigenetic regulation of white adipose tissue plasticity and energy metabolism by nucleosome binding HMGN proteins

Ravikanth Nanduri (), Takashi Furusawa, Alexei Lobanov, Bing He, Carol Xie, Kimia Dadkhah, Michael C. Kelly, Oksana Gavrilova, Frank J. Gonzalez and Michael Bustin ()
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Ravikanth Nanduri: National Institutes of Health
Takashi Furusawa: National Institutes of Health
Alexei Lobanov: National Institutes of Health
Bing He: National Institutes of Health
Carol Xie: National Institutes of Health
Kimia Dadkhah: Frederick National Laboratory for Cancer Research
Michael C. Kelly: Frederick National Laboratory for Cancer Research
Oksana Gavrilova: National Institutes of Health
Frank J. Gonzalez: National Institutes of Health
Michael Bustin: National Institutes of Health

Nature Communications, 2022, vol. 13, issue 1, 1-15

Abstract: Abstract White adipose tissue browning is a key metabolic process controlled by epigenetic factors that facilitate changes in gene expression leading to altered cell identity. We find that male mice lacking the nucleosome binding proteins HMGN1 and HMGN2 (DKO mice), show decreased body weight and inguinal WAT mass, but elevated food intake, WAT browning and energy expenditure. DKO white preadipocytes show reduced chromatin accessibility and lower FRA2 and JUN binding at Pparγ and Pparα promoters. White preadipocytes and mouse embryonic fibroblasts from DKO mice show enhanced rate of differentiation into brown-like adipocytes. Differentiating DKO adipocytes show reduced H3K27ac levels at white adipocyte-specific enhancers but elevated H3K27ac levels at brown adipocyte-specific enhancers, suggesting a faster rate of change in cell identity, from white to brown-like adipocytes. Thus, HMGN proteins function as epigenetic factors that stabilize white adipocyte cell identity, thereby modulating the rate of white adipose tissue browning and affecting energy metabolism in mice.

Date: 2022
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DOI: 10.1038/s41467-022-34964-5

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