期刊
GENES & DEVELOPMENT
卷 29, 期 3, 页码 298-307出版社
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.252734.114
关键词
PRDM16; PRDM3; MED1; Mediator; brown adipose tissue; UCP1
资金
- National Institute of General Medical Sciences/National Institutes of Health [DP2OD007288]
- Searle Scholars Award
- National Institutes of Health [R21DK098769]
- National Institute of Diabetes and Digestive and Kidney Diseases [R01 DK49780]
- JPB Foundation
PR (PRD1-BF1-RIZ1 homologous) domain-containing 16 (PRDM16) drives a brown fat differentiation program, but the mechanisms by which PRDM16 activates brown fat-selective genes have been unclear. Through chromatin immunoprecipitation (ChIP) followed by deep sequencing (ChIP-seq) analyses in brown adipose tissue (BAT), we reveal that PRDM16 binding is highly enriched at a broad set of brown fat-selective genes. Importantly, we found that PRDM16 physically binds to MED1, a component of the Mediator complex, and recruits it to superenhancers at brown fat-selective genes. PRDM16 deficiency in BAT reduces MED1 binding at PRDM16 target sites and causes a fundamental change in chromatin architecture at key brown fat-selective genes. Together, these data indicate that PRDM16 controls chromatin architecture and superenhancer activity in BAT.
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