BAF60a deficiency uncouples chromatin accessibility and cold sensitivity from white fat browning

Tongyu Liu, Lin Mi, Jing Xiong, Peter Orchard, Qi Yu, Lei Yu, Xu-Yun Zhao, Zhuo-Xian Meng, Stephen C. J. Parker, Jiandie D. Lin () and Siming Li ()
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Tongyu Liu: University of Michigan
Lin Mi: University of Michigan
Jing Xiong: University of Michigan
Peter Orchard: University of Michigan
Qi Yu: University of Michigan
Lei Yu: University of Michigan
Xu-Yun Zhao: University of Michigan
Zhuo-Xian Meng: Key Laboratory of Disease Proteomics of Zhejiang Province
Stephen C. J. Parker: University of Michigan
Jiandie D. Lin: University of Michigan
Siming Li: University of Michigan

Nature Communications, 2020, vol. 11, issue 1, 1-15

Abstract: Abstract Brown and beige fat share a remarkably similar transcriptional program that supports fuel oxidation and thermogenesis. The chromatin-remodeling machinery that governs genome accessibility and renders adipocytes poised for thermogenic activation remains elusive. Here we show that BAF60a, a subunit of the SWI/SNF chromatin-remodeling complexes, serves an indispensable role in cold-induced thermogenesis in brown fat. BAF60a maintains chromatin accessibility at PPARγ and EBF2 binding sites for key thermogenic genes. Surprisingly, fat-specific BAF60a inactivation triggers more pronounced cold-induced browning of inguinal white adipose tissue that is linked to induction of MC2R, a receptor for the pituitary hormone ACTH. Elevated MC2R expression sensitizes adipocytes and BAF60a-deficient adipose tissue to thermogenic activation in response to ACTH stimulation. These observations reveal an unexpected dichotomous role of BAF60a-mediated chromatin remodeling in transcriptional control of brown and beige gene programs and illustrate a pituitary-adipose signaling axis in the control of thermogenesis.

Date: 2020
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DOI: 10.1038/s41467-020-16148-1

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