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Series GSE26501 Query DataSets for GSE26501
Status Public on Jul 01, 2011
Title Regulation of nucleosome landscape and transcription factor binding at enhancers by BRG1
Organism Homo sapiens
Experiment type Genome binding/occupancy profiling by high throughput sequencing
Expression profiling by high throughput sequencing
Summary Enhancers of transcription activate transcription via binding of sequence-specific transcription factors to their target sites in chromatin. In this report, we identify GATA1-bound enhancers genome-wide and find a global reorganization of the nucleosomes at these enhancers during differentiation of hematopoietic stem cells (HSCs) to erythrocytes. We show that the catalytic subunit BRG1 of BAF complexes localizes to these enhancers during differentiation and generates a longer nucleosome repeat length surrounding the GATA1 sites by shifting the flanking nucleosomes away. Intriguing, we find that the nucleosome shifting specifically facilitates binding of TAL1 but not GATA1, which subsequently activates transcription of target genes.
 
Overall design Human hematopoietic stem cells (referred as CD34+ cells) were differentiated into erythroid lineage expressing the cell surface marker CD36 (referred as CD36+ cells). To study the function of ATP-dependent chromatin remodeling BAF complexes in the establishment of erythroid specific enhancers during differentiation, we mapped the genome-wide binding sites of GATA1 and TAL1, the key transcription regulators of erythroid differentiation, in CD36+ cells, then determined the genomic positions of the catalytic subunit BRG1 of the BAF complexes and the nucleosome landscapes, by ChIP-Seq and Mnase-Seq, respectively, for both HSCs and the differentiated cells. We compared changes in nucleosome landscapes with BRG1 binding at GATA1 and TAL1 binding sites and found that BRG1 binding is correlated with nucleosome shifting away from the binding sites, which is critical for TAL1 binding. To confirm that BRG1 is responsible for the nucleosome shift, we knocked down BRG1 in CD36+ cells and analyzed the nucleosome changes in the knockdown cells. The data indicated that inhibition of BRG1 caused a nucleosome shift towards the GATA1 or TAL1 sites, indicating that BRG1 is indeed responsible for the observed nucleosome shift.
 
Contributor(s) Hu G, Schones DE, Cui K, Ybarra R, Northrup D, Tang Q, Gattinoni L, Restifo NP, Huang S, Zhao K
Citation(s) 21795385, 27141965
Submission date Jan 07, 2011
Last update date May 15, 2019
Contact name Gangqing Hu
E-mail(s) michael.hu@hsc.wvu.edu
Organization name West Virginia University
Department MicroBiology, Immunology, and Cell Biology
Lab 2072A, HSC North, Floor 2
Street address 64 Medical Center Drive
City Morgantown
State/province West Virginia
ZIP/Postal code 26506-9177
Country USA
 
Platforms (1)
GPL9052 Illumina Genome Analyzer (Homo sapiens)
Samples (20)
GSM651541 CD34_WT_CTCF
GSM651542 CD36_shLuc_CTCF
GSM651543 CD36_shBrg1_CTCF
Relations
SRA SRP005281
BioProject PRJNA136673

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE26501_RAW.tar 4.9 Gb (http)(custom) TAR (of BED, TXT)
SRA Run SelectorHelp
Raw data are available in SRA
Processed data provided as supplementary file

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