Genomics

Dataset Information

96

EZH2-dependent chromatin accessibility changes during B cell differentiation


ABSTRACT: To understand the role of EZH2 in B cell differentiation, EZH2 was inducibly deleted using tamoxifen and B cells stimulated to differentiate with LPS in vivo. After 3 days, EZH2-sufficient and EZH2-deficient naive B cells and plasmablasts were FACS isolated from the spleens and ATAC-seq was performed to identify the chromatin accessibility changes that are programmed by EZH2. Overall design: Bone marrow chimeric mice were established from CD45.1/2 CRE negative and CD45.2 CRE positive Ezh2-floxed mice to study the cell intrinsic role of Ezh2 during B cell differentiaiton. Chimeric mice were treated with tamoxifen to induce deletion of Ezh2 in CD45.2 cells and subsequently inocculated with LPS to induce differentiation. Three-days later naïve B cells (nB) and differentiated plasmablasts (Pb) were isolated from Ezh2-sufficient (CD45.1/2) and Ezh2-deficient (CD45.2) populations by FACS.

INSTRUMENT(S): Illumina HiSeq 2500 (Mus musculus)

SUBMITTER: Chris Scharer  

PROVIDER: GSE103142 | GEO | 2017-12-16

SECONDARY ACCESSION(S): PRJNA400252

REPOSITORIES: GEO

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Publications

EZH2 Represses the B Cell Transcriptional Program and Regulates Antibody-Secreting Cell Metabolism and Antibody Production.

Guo Muyao M   Price Madeline J MJ   Patterson Dillon G DG   Barwick Benjamin G BG   Haines Robert R RR   Kania Anna K AK   Bradley John E JE   Randall Troy D TD   Boss Jeremy M JM   Scharer Christopher D CD  

Journal of immunology (Baltimore, Md. : 1950) 20171229 3


Epigenetic remodeling is required during B cell differentiation. However, little is known about the direct functions of epigenetic enzymes in Ab-secreting cells (ASC) in vivo. In this study, we examined ASC differentiation independent of T cell help and germinal center reactions using mice with inducible or B cell-specific deletions of Ezh2 Following stimulation with influenza virus or LPS, Ezh2-deficient ASC poorly proliferated and inappropriately maintained expression of inflammatory pathways,  ...[more]

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