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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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ChIP-seq based genome wide profiling of the histone mark H3K27ac and transcription factor Nuclear Factor 1 (NFI) in a differentiating murine brown preadipocyte cell line (IBA)

ABSTRACT: ChIP sequencing was used to generate genome-wide maps of the histone mark H3K27ac during in vitro differentiation of a murine brown preadipocyte cell line (IBA) at five different time points, in two biological replicates: Day 0 (confluence), 2h (post induction), Day 1, Day 2 and Day 4 (mature brown adipocytes). Additionally, transcription factor (TF) localisation maps of the Nuclear Factor 1 (NFI) were generated using ChIP sequencing at two time points: Day 0 and Day 4.

INSTRUMENT(S): NextSeq 550, Illumina HiSeq 2000

ORGANISM(S): Mus musculus

SUBMITTER: Rachana Pradhan

PROVIDER: E-MTAB-5159 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Dissecting the brown adipogenic regulatory network using integrative genomics.

Pradhan Rachana N RN Bues Johannes J JJ Gardeux Vincent V Schwalie Petra C PC Alpern Daniel D Chen Wanze W Russeil Julie J Raghav Sunil K SK Deplancke Bart B

Scientific reports 20170209

Brown adipocytes regulate energy expenditure via mitochondrial uncoupling, which makes them attractive therapeutic targets to tackle obesity. However, the regulatory mechanisms underlying brown adipogenesis are still poorly understood. To address this, we profiled the transcriptome and chromatin state during mouse brown fat cell differentiation, revealing extensive gene expression changes and chromatin remodeling, especially during the first day post-differentiation. To identify putatively causa ...[more]

PMID: 28181539

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mRNA-seq based gene expression profiling of differentiating murine brown preadipocytes (IBA)

Project description:mRNA-sequencing was used to profile temporal changes in gene expression during in vitro differentiation of IBA at five different time points: Day 0 (confluence), 2h (post induction), Day 1, Day 2 and Day 4 (mature brown adipocytes), performed in two biological replicates (with two technical replicates in the first biological replicate).

2017-10-14 | E-MTAB-5160 | biostudies-arrayexpress

Barcoded mRNA-seq of murine brown preadipocytes (IBA) upon transcriptomic perturbation

Project description:Loss of function assays were performed in differentiating IBAs using short hairpin RNAs (shRNAs) against a set of candidate transcription factors: NFIA, DBP, HOXA4, ZFP467, SOX18, ELF3, YBX2 and PPARa. Gene expression profiles of the perturbed and non perturbed (controls including non transduced cells, cells transduced with scrambled and GFP constructs) transcriptomes were measured at Day 6 of differentiation using a novel multiplex, bulk mRNA-seq barcoding method which employs a 3' sequencing approach. This method allowed the measurement of the deviation of the perturbed transcriptome from the non-perturbed transcriptome.

2017-09-21 | E-MTAB-5161 | biostudies-arrayexpress

Genome-wide maps of histone modification in WT and MLL4-/- during brown preadipocyte differentiation

Project description:Enhancers play a central role in cell-type-specific gene expression and are marked by H3K4me1/2. Active enhancers are further marked by H3K27ac. However, the methyltransferases responsible for the deposition of H3K4me1/2 on enhancers remain elusive. Furthermore, the functions of these methyltransferases on enhancers and associated cell-type-specific gene expression are poorly understood. Here, we identify MLL4 (KMT2D) as a major H3K4 mono- and di-methyltransferase in mammalian cells. Using adipogenesis and myogenesis as model systems, we show that MLL4 exhibits cell-type- and differentiation-stage-specific genomic binding and is predominantly localized on enhancers. MLL4 co-localizes with lineage-determining transcription factors (TFs) on active enhancers during differentiation. Deletion of MLL4 dramatically decreases H3K4me1/2 and H3K27ac on enhancers and leads to severe defects in cell-type-specific gene expression and cell differentiation. Finally, we provide evidence that lineage-determining TFs recruit and require MLL4 to establish enhancers critical for cell-type-specific gene expression. Together, these results identify MLL4 as an H3K4 mono-/di-methyltransferase required for enhancer activation during cell differentiation. ChIP-Seq analyses of histone modifications (H3K4me1, H3K4me2, H3K4me3, and H3K27ac) at D0 (day 0) and D2 (day 2) of adipogenesis in WT (MLL3-/-) and MLL4 KO (MLL3-/-;MLL4-/-) brown preadipocytes.

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2012-11-07 | E-GEOD-42018 | biostudies-arrayexpress

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Project description:Here we have characterized the transcriptional processes underlying the formation of human brown in white (i.e. brite) adipocytes using a genome-wide approach. We show that the browning process is associated with reprogramming of peroxisome proliferator-activated receptor γ (PPARγ) binding to form brite adipocyte-selective PPARγ super-enhancers that appear to play a key role in activation of brite adipocyte-selective genes. We identify the KLF11 gene based on its association with a PPARγ super-enhancer and show that KLF11 is a novel browning factor directly induced by rosiglitazone and required for the activation of brite adipocyte-selective gene program by rosiglitazone. Genome-wide profiling of Dnase I hypersenstive (DHS) sites, epigenomic marks, transcription factor and co-factor binding, and gene expression in hMADS white and brite adipocytes

2014-12-12 | E-GEOD-59703 | biostudies-arrayexpress

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2013-02-15 | E-GEOD-29898 | biostudies-arrayexpress

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