Single-nucleus RNA sequencing of mouse brown adipose tissue
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE207096 | GEO | 2022/07/03
REPOSITORIES: GEO
Similar Datasets
Project description:Brown adipose tissue (BAT) plays an essential role in metabolic homeostasis by dissipating energy via thermogenesis through uncoupling protein 1 (Ucp1). Previously, we reported that the TATA-binding protein Associated Factor 7L (Taf7l) is an important regulator of white adipose tissue (WAT) differentiation. Here, we show that Taf7l also serves as a molecular switch between brown fat and muscle lineages in vivo and in vitro. In adipose tissue, Taf7l containing TFIID complexes associate with PPAR to mediate DNA looping between distal enhancers and core promoter elements. Our findings suggest that presence of the tissue-specific Taf7l subunit in TFIID functions to promote long-range chromatin interactions during BAT lineage specification. mRNA-seq expression profiling wild type and Taf7l knockout interscapular brown adipose tissue (BAT)
2014-06-03 | E-GEOD-55797 | biostudies-arrayexpress
Project description:Obesity poses a global health challenge, demanding a deeper understanding of adipose tissue (AT) and its mitochondria. This study describes the role of the mitochondrial protein Methylation-controlled J protein (MCJ/DnaJC15) in orchestrating brown adipose tissue (BAT) thermogenesis. Here we show how MCJ expression decreases during obesity, as evident in human and mouse adipose tissue samples. MCJKO mice, even without UCP1, a fundamental thermogenic protein, exhibit elevated BAT thermogenesis. Electron microscopy unveils changes in mitochondrial morphology resembling BAT activation. Proteomic analysis confirms these findings and suggests involvement of the eIF2α mediated stress response. The pivotal role of eIF2α is scrutinized by in vivo CRISPR deletion of eIF2α in MCJKO mice, abrogating thermogenesis. These findings uncover the importance of MCJ as a regulator of BAT thermogenesis, presenting it as a promising target for obesity therapy.
2024-11-13 | PXD057026 | Pride
Project description:Various physiological stimuli, such as cold environment, diet, and hormones, trigger brown adipose tissue (BAT) to produce heat through sympathetic nervous system (SNS)- and -adrenergic receptors (ARs). The AR stimulation increases intracellular cAMP levels through heterotrimeric G proteins and adenylate cyclases, but the processes by which cAMP modulates brown adipocyte function are not fully understood. Here we described that specific ablation of cAMP production in brown adipocytes led to reduced lipolysis, mitochondrial biogenesis, uncoupling protein 1 (Ucp1) expression, and consequently defective adaptive thermogenesis. Elevated cAMP signaling by sympathetic activation inhibited Salt-inducible kinase 2 (Sik2) through protein kinase A (PKA)-mediated phosphorylation in brown adipose tissue. Inhibition of SIKs enhanced Ucp1 expression in differentiated brown adipocytes and Sik2 knockout mice exhibited enhanced adaptive thermogenesis at thermoneutrality in an Ucp1-dependent manner. Taken together, our data indicate that suppressing Sik2 by PKA-mediated phosphorylation is a requisite for SNS-induced Ucp1 expression and adaptive thermogenesis in BAT, and targeting Sik2 may present a novel therapeutic strategy to ramp up BAT thermogenic activity in humans.
2018-07-12 | PXD009262 | Pride
Project description:Brown adipose tissue (BAT) plays a central role in energy homeostasis through non-shivering thermogenesis. Besides, recent human studies using 18FDG-PET/CT imaging demonstrated that BAT acts as a significant metabolic-sink for glucose. Notably, these functions in BAT decrease with age: however what regulates this process remains poorly understood. To this end, we employed RNA-seq to identify the transcriptional changes in BAT of young and old mice.
2019-07-20 | E-MTAB-7445 | biostudies-arrayexpress
Project description:Brown adipose tissue (BAT) plays an essential role in metabolic homeostasis by dissipating energy via thermogenesis through uncoupling protein 1 (Ucp1). Previously, we reported that the TATA-binding protein Associated Factor 7L (Taf7l) is an important regulator of white adipose tissue (WAT) differentiation. Here, we show that Taf7l also serves as a molecular switch between brown fat and muscle lineages in vivo and in vitro. In adipose tissue, Taf7l containing TFIID complexes associate with PPAR to mediate DNA looping between distal enhancers and core promoter elements. Our findings suggest that presence of the tissue-specific Taf7l subunit in TFIID functions to promote long-range chromatin interactions during BAT lineage specification.
2014-06-03 | GSE55797 | GEO
Project description:The proteome cargo of extracellular vesicles released from brown adipose tissue (BAT) and from white adipose tissue (WAT) of mice subjected to cold exposure (4°C) was analysed by a TMT-based quantitative proteomic procedure in order to obtain new information on the processes of thermogenesis.
2022-05-20 | PXD026080 | Pride
Project description:We performed a genome-wide deep sequencing analysis of the microRNAs abundant in mesenchymal stem cells (MSCs) derived from murine brown adipose tissue and in in vitro differentiated mature brown adipocytes. Several microRNAs were identified as differentially regulated when comparing datasets from MSCs vs. mature fat cells. These microRNAs may have an implication in the regulation of adipogenesis as well as thermogenesis in brown adipose tissue (BAT). Examination of BAT-derived MSCs (BAT-MSC; 1 sample) and in vitro differentiated mature brown fat cells (BAT-DIFF; 1 sample) vertis biotechnologie AG, D-85354 Freising, Germany (library construction and sequencing)
2013-05-28 | E-GEOD-45499 | biostudies-arrayexpress
Project description:Thermogenesis is a promising approach to limit weight gain in response to excess nutrition. In contrast to cold-induced thermogenesis, the molecular and cellular mechanisms of diet-induced thermogenesis (DIT) have not been fully characterized. Here, we explored the response of brown adipose tissue (BAT) and beige adipose tissue to high fat diet (HFD) using proteome and phosphoproteome analysis. We observed that after HFD, DIT was only activated in BAT. Furthermore, fatty acid oxidation, tricarboxylic acid cycle, and oxidative phosphorylation were also activated in BAT. Nevertheless, most metabolic pathways downregulated in beige adipose tissue. Strikingly, we found that these metabolic changes accompanied with different variation of mitochondria between BAT and beige adipose tissue as well. HFD treatment impaired mitochondrial functions and mitochondrial protein synthesis in beige adipose tissue while it stimulated mitochondrial autophagy in BAT. Together, in BAT, HFD caused increased mitochondrial activity,
2022-04-01 | PXD032888 |
Project description:The coexistence of brown adipocytes with low and high thermogenic activity is a fundamental feature of brown adipose tissue (BAT) heterogeneity and plasticity. However, the mechanisms that govern thermogenic adipocyte heterogeneity and its significance in obesity and metabolic disease remain poorly understood. Here we show that in male mice, a population of JunB-enriched (JunB+) adipocytes within the BAT exhibits lower thermogenic capacity compared to high-thermogenic adipocytes. To determine if JunB plays a role in the control of brown adipocyte heterogeneity in thermogenesis, we performed single-nucleus RNA sequencing (snRNA-seq) of BAT from JunB FKO and control mice (3-month-old male mice (5/group)) housed at room temperature. Our study pointing to a potent inhibition by JunB in the conversion from low- to high-thermogenic adipocyte.
2023-10-03 | GSE244239 | GEO
Project description:Adrenergic stimulation of brown adipose tissue (BAT) activates thermogenesis, by uncoupling oxidative phosphorylation and enabling high rates of substrate oxidation. Moreover, adrenergic stimulation signals to the nucleus, inducing gene expression changes that increase BAT thermogenic and oxidative capacity. The purpose of this study was to determine the role of two orphan nuclear receptors, ERRα and ERRγ, in adipose tissue function in response to adrenergic stimulation. Here we identify ERRα and ERRγ as collectively critical effectors of the adrenergic induced transcriptional program in BAT. Mice lacking adipose ERRs (ERRαγAd-/-) have diminished oxidative and thermogenic capacity, and become rapidly hypothermic when exposed to cold. Notably, the ability of the β3-adrenergic agonist CL316,243 to expand BAT oxidative and thermogenic capacity, increase energy expenditure, promote weight loss, and improve glucose tolerance is lost in ERRαγAd-/-. At the transcriptional level, RNA sequencing experiments show that the bulk of the response of BAT to CL316,243 (>80% of CL316,243-induced genes) relies on ERRs. These findings establish ERRα and ERRγ as essential BAT regulators that act coordinately to relay adrenergic signals and expand the capacity for thermogenesis and energy expenditure.
2018-03-19 | GSE104285 | GEO