Project description:We used the dTAG protein degradation system to rapidly deplete transcription factor EBF1 in the B cell culture. After treatment with dTAG-13 for 6 hours, we performed ChIP-seq, ATAC-seq, and RNA-seq. After the treatment, EBF1 is completely absent from the chromatin. This leads to the closure of EBF1 binding sites and changes in the target gene expression. This approach allowed us to identify direct targets of EBF1 and show the importance of EBF1 for open chromatin maintenance.
Project description:We used the dTAG protein degradation system to rapidly deplete transcription factor EBF1 in the B cell culture. After treatment with dTAG-13 for 6 hours, we performed ChIP-seq, ATAC-seq, and RNA-seq. After the treatment, EBF1 is completely absent from the chromatin. This leads to the closure of EBF1 binding sites and changes in the target gene expression. This approach allowed us to identify direct targets of EBF1 and show the importance of EBF1 for open chromatin maintenance.
Project description:We used the dTAG protein degradation system to rapidly deplete transcription factor EBF1 in the B cell culture. After treatment with dTAG-13 for 6 hours, we performed ChIP-seq, ATAC-seq, and RNA-seq. After the treatment, EBF1 is completely absent from the chromatin. This leads to the closure of EBF1 binding sites and changes in the target gene expression. This approach allowed us to identify direct targets of EBF1 and show the importance of EBF1 for open chromatin maintenance.
Project description:EBF1 is essential for B cell specification and commitment. To explore the dynamics of EBF1 initiated B cell programming, we performed EBF1 ChIP-seq, ATAC-seq, bisulfite-seq, RNA-seq and several histone ChIP-seq analyses at different stages of the transition from Ebf1-/- pre-pro-B to pro-B triggered by EBF1 restoration. We also performed Pax5 ChIP-seq in Ebf1-/- pre-pro-B cell and EBF1-restored pro-B cell to study the pioneering function of EBF1 that allows other transcription factors to access certain chromatin sites.
Project description:EBF1 is essential for B cell specification and commitment. To explore the dynamics of EBF1 initiated B cell programming, we performed EBF1 ChIP-seq, ATAC-seq, bisulfite-seq, RNA-seq and several histone ChIP-seq analyses at different stages of the transition from Ebf1-/- pre-pro-B to pro-B triggered by EBF1 restoration. We also performed Pax5 ChIP-seq in Ebf1-/- pre-pro-B cell and EBF1-restored pro-B cell to study the pioneering function of EBF1 that allows other transcription factors to access certain chromatin sites.
Project description:ChIP-seq data from mouse adipocyte. Mature 3T3-L1 adipocytes were cross-linked with 1% formaldehyde 10 days after induction with MDI. Frozen cell pellets were submitted to the Broad Institute for subsequent analysis of Ebf1-bound regions using anti-Ebf1 antibody (Abnova H00001879-M01).
Project description:Ebf1 is a key determinant of B-lymphocyte specification. In order to identify unknown transcriptional targets, endogenous Ebf1 was isolated by chromatin-IP from primary pro-B cells and the copurified DNA was hybridized to promoter tiling arrays. Ebf1 was ChIPed using a polyclonal antibody directed against an N-terminal peptide from primary pro-B cells grown in the presence of Il7. The resulting DNA was analyzed by tiling array hybridization.
