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Shared PPARα/γ target genes regulate brown adipocyte thermogenic function

ABSTRACT: Shared PPARα/γ target genes regulate brown adipocyte thermogenic function

PROVIDER: PRJNA603779 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10985432_1.fastq.gz	Fastqsanger.gz
	SRR10985432_2.fastq.gz	Fastqsanger.gz
	SRR10985433_1.fastq.gz	Fastqsanger.gz
	SRR10985433_2.fastq.gz	Fastqsanger.gz
	SRR10985434_1.fastq.gz	Fastqsanger.gz

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Shared PPARα/γ target genes regulate brown adipocyte thermogenic function (RNA-Seq)

Project description:Shared PPARα/γ target genes regulate brown adipocyte thermogenic function (RNA-Seq)

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The shared PPARα/γ target genes regulate brown adipocyte thermogenic function (ChIP-Seq)

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The shared PPARα/γ target genes regulate brown adipocyte thermogenic function (ChIP-Seq)

Project description:We report the application of sequencing technology for high-throughput profiling of PPARα/γ in mammalian cells. By obtaining over 3 billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of mouse brown adipose tissue. We find that PPARα binds to a subset of PPARγ sites, suggesting a potential redundancy in which PPARα function may not be necessary in brown adipose tissue.While PPARα may not itself be necessary for BAT function, shared targets regulation by PPARα and PPARγ may nonetheless reveal relevant biology in this tissue.This study provides a framework for the application of comprehensive chromatin profiling towards characterization of PPARα/γ regulation in mouse brown adipose tissue.

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Shared PPARα/γ target genes regulate brown adipocyte thermogenic function (RNA-Seq)

Project description:Purpose: To study the role of PPAR nuclear receptors in brown fat. Methods: mRNA-sequencing was performed on brown adipose tissue from mice on diets with or without added rosiglitazone or fenofibrate. Sequence reads that passed quality filters were analyzed at the transcript isoform level with RNA-Seq Unified Mapper. Results: We identified genes that were induced or repressed by either PPAR agonist, and approximately three-fold more genes were significantly regulated by rosiglitazone (rosi, a PPARg agonist) than by fenofibrate (feno, a PPARa agonist). Those genes induced by either drug were enriched for expected lipid metabolic pathways, while down-regulated genes fell in pathways of uncertain relevance. Most genes were selectively regulated by one of the two PPAR agonists, with few regulated by both. Only 34 genes were induced by both PPAR agonists (~10% of rosi-induced genes and ~25% of feno-induced genes), and these were enriched for mitochondrial functionrelated pathways, including fatty acid β-oxidation. Conclusions: These data suggest that PPARγ agonists have stronger effects on BAT than PPARα agonists, yet those genes activated by both PPAR agonists may be particularly relevant to BAT function.

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Shared PPARα/γ target genes regulate brown adipocyte thermogenic function

Project description:This SuperSeries is composed of the SubSeries listed below.

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BCL6 reinforces brown adipocyte cellular identity to preserve thermogenic fitness

Project description:Brown adipose tissue (BAT) generates heat via uncoupled respiration, providing mammals with an evolutionary defense against environmental cold. Although the molecular pathways by which cold activates brown adipocytes are well understood, little is known about how BAT maintains its thermogenic capacity during adaptation to environmental warmth. Here, we identify the transcriptional repressor BCL6 as the switch for maintaining brown adipocyte cellular identity under warm conditions. Mice lacking BCL6 in their brown adipocytes display normal thermogenic responses when housed in a cool environment, but fail to maintain thermogenic fitness when housed under warm conditions. In a temperature-dependent manner, BCL6 suppresses apoptosis, fatty acid storage, and coupled respiration to maintain thermogenic competence in brown adipocytes. Enhancer analysis revealed that BCL6 reinforces brown-specific while opposing white-specific enhancers to maintain cellular identity. Thus, unlike other regulators, BCL6 is dispensable for differentiation and activation of brown adipocytes, but specifically required for their maintenance in warmth.

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BCL6 reinforces brown adipocyte cellular identity to preserve thermogenic fitness

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