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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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

ABSTRACT: 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).

INSTRUMENT(S): NextSeq 550, Illumina HiSeq 2000

ORGANISM(S): Mus musculus

SUBMITTER: Rachana Pradhan

PROVIDER: E-MTAB-5160 | 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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Project description: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.

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2016-01-18 | E-GEOD-76881 | biostudies-arrayexpress

Genome-wide maps of 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 MLL4 binding profiles at D0 (day 0), D2 (day 2), and D7 (day 7) of adipogenesis in WT (MLL3-/-) and MLL4 KO (MLL3-/-;MLL4-/-) brown preadipocytes. D0 and D2 input DNA samples can be found in GSE50417.

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Protein SUMOylation is required for regulatory T cell expansion and function

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RNA-seq of the zebrafish (danio rerio) brain after developmental exposure to 17-ethinylestradiol

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2017-10-02 | E-MTAB-5173 | biostudies-arrayexpress

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2016-02-11 | E-GEOD-76117 | biostudies-arrayexpress

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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. RNA-Seq analyses of mRNA profiles at D0 (day 0) and D2 (day 2) of adipogenesis in WT (MLL3-/-) and MLL4 KO (MLL3-/-;MLL4-/-) brown preadipocytes.

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