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Cebpa in adipocyte differentiation

ABSTRACT: Cebpa in adipocyte differentiation

PROVIDER: PRJNA923017 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23054527.fastq.gz	Fastqsanger.gz
	SRR23054528.fastq.gz	Fastqsanger.gz
	SRR23054529.fastq.gz	Fastqsanger.gz
	SRR23054530.fastq.gz	Fastqsanger.gz
	SRR23054531.fastq.gz	Fastqsanger.gz

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Chromatin interaction of Cebpa during adipocyte differentiation (4C-Seq)

Project description:Cebpa is a critical transcription factor gene for adipocyte differentiation and adipose tissue development. However, mechanisms controlling Cebpa expression during adipogenic differentiation remain largely unknown. Here, we generated the high-resolution chromatin interaction maps of Cebpa in 3T3-L1 preadipocytes (3T3-L1) and 3T3-L1 adipocytes (3T3-L1-AD) using circularized chromosome conformation capture coupled with next-generation sequencing (4C-seq), and characterized differences in their chromatin interactomes and chromatin status of the interaction sites during adipogenic differentiation. We performed a 4C-seq experiment on inguinal white adipose tissue (iWAT) to evaluate whether chromatin interaction between Cebpa-L1-AD-En2 and Cebpa promoters in 3T3-L1 adipocytes also exists in mouse adipose tissue.

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Chromatin interaction of Cebpa during adipocyte differentiation (4C-Seq)

Project description:Chromatin interaction of Cebpa during adipocyte differentiation (4C-Seq)

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Identifying functional enhancers regulating Cebpa expression and adipocyte differentiation (mRNA-Seq)

Project description:Identifying functional enhancers regulating Cebpa expression and adipocyte differentiation (mRNA-Seq)

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Integrated analysis of transcript level regulation of metabolism during human adipocyte differentiation [ChIP-Seq]

Project description:Here, we have focused on studying the link between metabolic changes driven by the differentiation into mature adipocytes of a human preadipocyte cell line (SGBS) and their regulation, through a combined experimental and computational approach. By collecting data on gene expression, PPARg, CEBPa, LXR and H3K4me3 genome-wide ChIP-seq profles and transcriptome-wide microRNA target identification for miR-27a, miR29a and miR-222, and using constraint-based modeling to estimate metabolic reaction activity, we obtained a comprehensive set of information highlighting how epigenetic, transcriptional and post-transcriptional regulation impacts the metabolic network. Illumina Solexa sequencing: Six samples in total. Two ChIP-seq samples were prepared using an antibody against H3K4me3 active TSS chromatin marker from human SGBS preadipocyte and day 10 differentiated SGBS adipocyte cells. From day 10 differentiated SGBS cells additional three samples were prepared using an antibody against PPARg, CEBPa and LXRa to determine their genome-wide binding. One input control sample is included.

2013-11-19 | E-GEOD-41629 | biostudies-arrayexpress

Identifying functional enhancers regulating Cebpa expression and adipocyte differentiation (mRNA-Seq)

Project description:To explore the effect of enhancer repression on adipocyte differentiation in a transcriptome-wide manner, we infected cells with 1 mL lentiviruses medium containing dCas9-KRAB-En2-sgRNAs (Experimental group) or dCas9-KRAB (Control group) at the multiplicity of infection (MOI) of 100 for 12 h. We performed transcriptional profiling by RNA sequencing (RNA-seq) for dCas9-KRAB-En2 and dCas9-KRAB cells at day 7 of differentiation.

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Dual Functions of TAF7L in Adipocyte Differentiation

Project description:The diverse transcriptional mechanisms governing cellular differentiation and development of mammalian tissue remains poorly understood. Here we report that TAF7L, a paralogue of TFIID subunit TAF7, is enriched in adipocytes and mouse white fat tissue (WAT). Depletion of TAF7L reduced adipocyte-specific gene expression and compromised adipocyte differentiation as well as WAT development. Ectopic expression of TAF7L in myoblasts reprograms these muscle precursors into adipocytes upon induction. Genome-wide mRNA-seq expression profiling and ChIP-seq binding studies confirmed that TAF7L is required for activating adipocyte-specific genes via a dual mechanism wherein it interacts with PPARM-NM-3 at enhancers and TBP/Pol II at core promoters. In vitro binding studies confirmed that TAF7L forms complexes with both TBP and PPARM-NM-3. These findings suggest that TAF7L plays an integral role in adipocyte gene expression by targeting enhancers as a cofactor for PPARM-NM-3 and promoters as a component of the core transcriptional machinery. Genome-wide mapping of TAF7L and additional factors, and mRNA-seq expression profiling prior to and following mouse adipocyte differentiation.

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Transcription profiling of mouse 3T3-L1 adipocyte differentiation time series-3T3-L1 adipocyte differentiation timeseries

Project description:3T3-L1 adipocyte differentiation time series-3T3-L1 adipocyte differentiation timeseries. Hackl H*, Burkard T*, Sturn A, Rubio R, Schleiffer A, Tian S, Quackenbush J, Eisenhaber F, Trajanoski Z. Molecular processes during fat cell development revealed by gene expression profiling and functional annotation. Genome Biol. 2005. 6:R108.

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Enhancer and transcription factor dynamics within the granulocytic-monocytic lineage reveal an early differentiation block in Cebpa null progenitors

Project description:Myeloid cells of the granulocytic-monocytic (GM) lineage develop in a process orchestrated mainly by the transcription factors PU.1 and CEBPA, but how these factors collaborate on a global scale during GM-lineage differentiation remains uncharacterized. To address this question we have combined epigenetic profiling, transcription factor binding and gene expression analyses of successive stages of murine GM-lineage differentiation and show that PU.1 and CEBPA binds to GM enhancers with distinct kinetics. Surprisingly, we find no evidence of a pioneering function of PU.1 during GM-lineage differentiation but instead delineate a set of GM enhancers that appears to open in a CEBPA-dependent manner. Analyses of Cebpa null bone marrow demonstrate that CEBPA controls PU.1 levels and, unexpectedly, that the loss of CEBPA results in a very early differentiation block. These data are consistent with a model involving an extensive functional interplay between PU.1 and CEBPA in driving GM-lineage differentiation.

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