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ChIP-sequence analysis of H3K27ac, H3K4me1, and SETD5 in 3T3-L1 preadipocytes.

ABSTRACT: ChIP-sequence analysis of H3K27ac, H3K4me1, and SETD5 in 3T3-L1 preadipocytes.

PROVIDER: PRJNA762097 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15834019.fastq.gz	Fastqsanger.gz
	SRR15834020.fastq.gz	Fastqsanger.gz
	SRR15834021.fastq.gz	Fastqsanger.gz
	SRR15834022.fastq.gz	Fastqsanger.gz
	SRR15834023.fastq.gz	Fastqsanger.gz

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Expression data from SETD5-expressing 3T3-L1 cells; ChIP-seq of H3K27ac, H3K4me1, and SETD5 in 3T3-L1 preadipocytes.

Project description:Expression data from SETD5-expressing 3T3-L1 cells; ChIP-seq of H3K27ac, H3K4me1, and SETD5 in 3T3-L1 preadipocytes.

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ChIP-sequence analysis of H3K27ac, H3K4me1, and SETD5 in 3T3-L1 preadipocytes.

Project description:Enhancer activation is essential for cell-type specific gene expression during cellular differentiation, however, how enhancers transition from a hypoacetylated “primed” state to a hyperacetylated-active state is incompletely understood. Here, we show SET domain-containing 5 (SETD5) forms a complex with NCoR-HDAC3 co-repressor that prevents histone acetylation of enhancers for two master adipogenic regulatory genes Cebpa and Pparg early during adipogenesis. The loss of SETD5 from the complex is followed by enhancer hyperacetylation. SETD5 protein levels were transiently increased and rapidly degraded prior to enhancer activation providing a mechanism for the loss of SETD5 during the transition. We show that induction of the CDC20 co-activator of the ubiquitin ligase leads to APC/C mediated degradation of SETD5 during the transition and this operates as a molecular switch that facilitates adipogenesis.

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Expression data from SETD5-expressing 3T3-L1 cells.

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LSD1 knockdown in 3T3-L1 preadipocytes

Project description:Obesity is often associated with a low-grade systemic inflammation state that contributes to the development of insulin resistance and atherosclerotic complications. This is usually coupled with increased macrophage infiltration in the adipose tissue and a defect in adipocyte differentiation that results in accumulation of hypertrophic fat cells characterized by a deregulated pattern of adipokine expression. Here we show that knockdown of histone demethylase lsd1 in 3T3-L1 preadipocytes results in defective adipogenesis and derepression of an inflammatory program in these cells. The dataset consists of four sample groups: [1] 3T3-L1 preadipocytes (passage 19) transfected with a control scrambled siRNA at 24h after transfection (siC.24h), [2] 3T3-L1 preadipocytes (p.19) transfected with a siRNA directed against LSD1 at 24h after transfection (siLsd1.24h), [3] 3T3-L1 preadipocytes (p.21) transfected with a control scrambled siRNA at 48h after transfection (siC.48h), and [4] 3T3-L1 preadipocytes (p.21) transfected with a siRNA directed against LSD1 at 48h after transfection (siLsd1.48h). The 24h sample groups (siC.24h and siLsd1.24h) consist of two biological replicate samples; the 48h sample groups (siC.48h and siLsd1.48h) consist of three biological replicate samples. Each sample was hybridized to a separate array, for a total of ten arrays.

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Expression data from SETD5-expressing 3T3-L1 cells; ChIP-seq of H3K27ac, H3K4me1, and SETD5 in 3T3-L1 preadipocytes.

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

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Whole genome bisulfite sequencing of 3T3-L1 preadipocytes and adipocytes

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Expression data from 3T3-L1 preadipocytes and 10Thalf mesenchymal stem cells

Project description:Bivalent H3K4me3 and H3K27me3 chromatin domains in embryonic stem cells keep active developmental regulatory genes expressed at very low levels and poised for activation. Here, we show an alternative and previously unknown bivalent modified histone signature in lineage-committed mesenchymal stem cells and preadipocytes that pairs H3K4me3 with H3K9me3 to maintain adipogenic master regulatory genes (Cebpa and Pparg) expressed at low levels yet poised for activation when differentiation is required. We show lineage-specific gene-body DNA methylation recruits H3K9 methyltransferase SETDB1 which methylates H3K9 immediately downstream of transcription start sites marked with H3K4me3 to establish the bivalent domain. At the Cebpa locus, this prevents transcription factor C/EBPÎ² binding, histone acetylation, and further H3K4me3 deposition and is associated with pausing of RNA polymerase II, which limits Cebpa gene expression and adipogenesis. We used microarrays to detail the global programme of gene expression in 3T3-L1 preadipocytes and 10Th1lf mesenchymal stem cells and identified up-regulated genes upon knockdown of SETDB1, MBD1, and MCAF1. SETDB1, MBD1, or MCAF1 was knocked-down in 3T3-L1 preadipocytes and 10Thalf mesenchymal stem cells for RNA extraction and hybridization on Affymetrix microarrays. Small interfering RNAs (siRNA) targeting to Setdb1, Mbd1, or Mcaf1 was transfected to 3T3-L1 preadipocytes or 10Thalf mesenchymal stem cells.

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Expression data from SETD5-expressing 3T3-L1 cells.

Project description:Expression data from SETD5-expressing 3T3-L1 cells.

| PRJNA762098 | ENA