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Publication : PRDM16 binds MED1 and controls chromatin architecture to determine a brown fat transcriptional program.

First Author  Harms MJ Year  2015
Journal  Genes Dev Volume  29
Issue  3 Pages  298-307
PubMed ID  25644604 Mgi Jnum  J:218231
Mgi Id  MGI:5617061 Doi  10.1101/gad.252734.114
Citation  Harms MJ, et al. (2015) PRDM16 binds MED1 and controls chromatin architecture to determine a brown fat transcriptional program. Genes Dev 29(3):298-307
abstractText  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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