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BRD4 directs glycolytic metabolism through a comprehensive epigenomic and transcriptional network

ABSTRACT: BRD4 directs glycolytic metabolism through a comprehensive epigenomic and transcriptional network

PROVIDER: PRJNA254508 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1508390_1.fastq.gz	Fastqsanger.gz
	SRR1508390_2.fastq.gz	Fastqsanger.gz
	SRR1508400_1.fastq.gz	Fastqsanger.gz
	SRR1508400_2.fastq.gz	Fastqsanger.gz
	SRR1508391_1.fastq.gz	Fastqsanger.gz

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BRD4 directs glycolytic metabolism through a comprehensive epigenomic and transcriptional network

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Enhancer-binding of Brd4 controls cell differentiation

Project description:The epigenomic reader Brd4 is an important drug target for cancers. However, its role in cell differentiation and animal development remains largely unclear. Using two conditional knockout mouse strains and derived cells, we demonstrate that Brd4 controls cell identity gene induction and is essential for adipogenesis and myogenesis. Brd4 co-localizes with lineage-determining transcription factors (LDTFs) on active enhancers during differentiation. LDTFs coordinate with H3K4 mono-methyltransferases MLL3/MLL4 (KMT2C/KMT2D) and H3K27 acetyltransferases CBP/p300 to recruit Brd4 to enhancers activated during differentiation. Brd4 deletion prevents the enrichment of Mediator and RNA polymerase II transcription machinery, but not that of LDTFs, MLL3/MLL4-mediated H3K4me1, and CBP/p300-mediated H3K27ac, on enhancers. Consequently, Brd4 deletion prevents enhancer RNA production, cell identity gene induction and cell differentiation. Interestingly, Brd4 is dispensable for maintaining cell identity genes in differentiated cells. These findings identify Brd4 as an enhancer epigenomic reader that links active enhancers with cell identity gene induction in differentiation.

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BRD4 links carbohydrate and lipid synthetic pathways to a core transcriptional network for a cell-type specific metabolic response (RNA-seq Fat)

Project description:Glucose and fat metabolism are tightly interconnected where endogenous de novo lipogenesis (DNL) serves to convert carbohydrates directly into lipids. Here, we explored the role of the long isoform Brd4 as a key transcriptional co-activator in lipogenesis. As a member of the Bromo-extraterminal (BET) protein family, Brd4 is characterized by two tandem bromodomains that bind acetylated lysine on both histone and non-histone proteins in chromatin. We found that treatment with MS417, a small molecule inhibitor of Brd4 binding to acetylated lysine, suppresses 3T3-L1 adipocyte differentiation. MS417-treated obese (ob/ob) mice displayed resistance to weight gain and loss of fat from steatotic livers. Comprehensive RNA-seq and ChIP-seq analyses delineate a Brd4-driven gene network required for glycolysis-lipogenesis flux that is shared between glycolytic liver and 3T3-L1 adipocytes, but absent in the non-glycolytic white abdominal fat. Our data further reveal that Brd4 functions to provide specific metabolic resources, such as acetyl-CoA and nicotinamide adenine dinucleotide (NAD) cofactors, in cell types utilizing DNL. Collectively, these findings provide a novel view of the critical role Brd4 plays in orchestrating transcription of a network of genes directing metabolic pathways governing carbohydrate fueled lipid metabolism fundamental for controlling glucose homeostasis and body weight.

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