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Enhancer retargeting at the PAX5/ZCCHC7 locus

ABSTRACT: Enhancer retargeting at the PAX5/ZCCHC7 locus

PROVIDER: PRJNA868184 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21001931_1.fastq.gz	Fastqsanger.gz
	SRR21001931_2.fastq.gz	Fastqsanger.gz
	SRR21001932_1.fastq.gz	Fastqsanger.gz
	SRR21001932_2.fastq.gz	Fastqsanger.gz
	SRR21001933_1.fastq.gz	Fastqsanger.gz

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Enhancer retargeting at the PAX5/ZCCHC7 locus

Project description:2 kinds of SU-DHL-10 cell clones (Pax5-TSS2mut/deletion) were generated to investigate enhancer relocation, we campared 4C-seq data between the Pax5-TSS2mut/deletion clones and wild type SU-DHL-10.

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Enhancer Release and Retargeting” Activates Disease Susceptibility Genes

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Wapl repression by Pax5 promotes loop extrusion and V gene recombination at the Igh locus

Project description:The generation of a diverse antibody repertoire is essential for humoral immunity and requires the participation of all V genes in V(D)J recombination, which depends on the Pax5-regulated contraction of the 2.8-Mb long immunoglobulin heavy-chain (Igh) locus. How Pax5 controls Igh contraction in pro-B cells is, however, not known. Here, we demonstrate that locus contraction is caused by cohesin-mediated chromatin loop extrusion across the entire Igh locus. Notably, expression of the cohesin-release factor Wapl is repressed by Pax5 specifically in pro-B and pre-B cells, which facilitates extended loop extrusion by increasing the residence time of cohesin on chromatin. Pax5 mediates the transcriptional repression of Wapl through a single Pax5-binding site by recruiting the Polycomb repressive complex 2 to induce bivalent chromatin at the Wapl promoter. Reduced Wapl expression causes global alterations of the three-dimensional chromatin architecture, indicating that the potential to recombine all V genes entails structural changes of the entire genome in pro-B cells.

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Enhancer Release and Retargeting” Activates Disease Susceptibility Genes (GRO-Seq)

Project description:Enhancer Release and Retargeting” Activates Disease Susceptibility Genes (GRO-Seq)

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Enhancer Release and Retargeting” Activates Disease Susceptibility Genes (ChIP-Seq)

Project description:Enhancer Release and Retargeting” Activates Disease Susceptibility Genes (ChIP-Seq)

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IGH analysis in pro-B cells with H3K4me3, H3K4me2, H3K9ac, H3K27me3, Pax5 and CTCF [ChIP-Seq]

Project description:VH-DJH recombination of the immunoglobulin heavy-chain (Igh) locus is temporally and spatially controlled during early B-cell development, and yet no regulatory elements other than the VH gene promoters have been identified throughout the entire 2.5-Mb VH gene cluster. Here we discovered novel regulatory sequences that are interspersed in the distal VH gene region. These conserved repeat elements were characterized by the presence of Pax5-dependent active chromatin, the binding of Pax5, E2A, CTCF and Rad21 as well as by Pax5-dependent antisense transcription in pro-B cells. The Pax5-activated intergenic repeat (PAIR) elements were no longer bound by Pax5 in pre-B and B cells consistent with the loss of antisense transcription, whereas E2A and CTCF interacted with PAIR elements throughout early B-cell development. The pro-B-cell-specific and Pax5-dependent activity of the PAIR elements suggests that they are involved in the regulation of distal VH-DJH recombination at the Igh locus. Analysis of chromatin and TF binding in rag2-/- and wt pro-B, DP T and Mature B cells. Chip-Seq of CTCF and Rad21. The provided data is in mm8 coordinates.

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