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ABSTRACT: RAG-mediated DNA breaks attenuate PU.1 activity in early B cells through activation of a SPIC-BCLAF1 complex

PROVIDER: PRJNA527987 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8750170.fastq.gz	Fastqsanger.gz
	SRR8750171.fastq.gz	Fastqsanger.gz
	SRR8750162.fastq.gz	Fastqsanger.gz
	SRR8750172.fastq.gz	Fastqsanger.gz
	SRR8750163.fastq.gz	Fastqsanger.gz

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Similar Datasets

RAG-mediated DNA breaks attenuate PU.1 activity in early B cells through activation of a SPIC-BCLAF1 complex

Project description:RAG-mediated DNA breaks attenuate PU.1 activity in early B cells through activation of a SPIC-BCLAF1 complex

| PRJNA530207 | ENA

RAG-mediated DNA breaks attenuate PU.1 activity in early B cells through activation of a SPIC-BCLAF1 complex [RNA-Seq]

Project description:RAG DSBs trigger ATM-dependent induction of SPIC, an ETS family transcriptional repressor with significant homology to PU.1. RAG DSB-mediated expression of SPIC results in displacement of PU.1 throughout the genome and induction of broad transcriptional changes in pre B cells. SPIC also binds and recruits a unique partner, BCLAF1 to gene regulatory elements that regulate expression of key B cell developmental genes.

2019-08-22 | GSE129129 | GEO

RAG-mediated DNA breaks attenuate PU.1 activity in early B cells through activation of a SPIC-BCLAF1 complex [ChIP-Seq]

2019-08-22 | GSE129124 | GEO

RAG-mediated DNA double strand breaks activate a cell-type-specific checkpoint to inhibit pre-B cell receptor signals

Project description:Pre-B cell receptor (pre-BCR) signals initiate immunoglobulin light (Igl) chain gene assembly leading to RAG-mediated DNA double-strand breaks (DSBs). These signals also promote cell cycle entry, which could cause aberrant DSB repair and genome instability in pre-B cells. Here we show that RAG DSBs inhibit pre-BCR signals through the ATM- and NF-κB2-dependent induction of SPIC, a hematopoietic-specific transcriptional repressor. SPIC inhibits expression of the SYK tyrosine kinase and BLNK adaptor to prevent the pre-BCR from inducing additional Igl chain gene rearrangements and driving pre-B cells with RAG DSBs into cycle. We propose that pre-B cells toggle between pre-BCR signals and this RAG DSB-dependent checkpoint to maintain genome stability while iteratively assembling Igl chain genes.

2016-01-13 | GSE67854 | GEO

RAG-mediated DNA double strand breaks activate a cell-type-specific checkpoint to inhibit pre-B cell receptor signals

Project description:Pre-B cell receptor (pre-BCR) signals initiate immunoglobulin light (Igl) chain gene assembly leading to RAG-mediated DNA double-strand breaks (DSBs). These signals also promote cell cycle entry, which could cause aberrant DSB repair and genome instability in pre-B cells. Here we show that RAG DSBs inhibit pre-BCR signals through the ATM- and NF-ÎºB2-dependent induction of SPIC, a hematopoietic-specific transcriptional repressor. SPIC inhibits expression of the SYK tyrosine kinase and BLNK adaptor to prevent the pre-BCR from inducing additional Igl chain gene rearrangements and driving pre-B cells with RAG DSBs into cycle. We propose that pre-B cells toggle between pre-BCR signals and this RAG DSB-dependent checkpoint to maintain genome stability while iteratively assembling Igl chain genes. Three independent IL-7 cultures for each genotype (Rag1-/-:Î¼IgH:Bcl2, Art-/-:Î¼IgH:Bcl2 and Art-/-:Nfkb2-/-:Î¼IgH:Bcl2) were withdrawn from IL-7 for 2 days. RNA was isolated using RNeasy (Qiagen). Gene expression profiling was performed using Illumina MouseRef-8 expression microarrays.

2016-01-13 | E-GEOD-67854 | biostudies-arrayexpress

On-target and Off-target Activities of RAG Are Restricted by Topological Chromatin Domains

Project description:RAG initiates V(D)J recombination in developing lymphocytes by generating "on-target" DNA double-stranded breaks at bona fide recombination signal sequence (RSS) pairs. We now employ RAG-generated DNA breaks in endogenous or ectopically-inserted RSS pairs as bait to identify huge numbers of RAG "off-target" sites. These off-target DNA breaks occur across convergent CTCF-binding element (CBE)-flanked loop domains containing the bait RSS pairs. Such off-target cleavage occurs at the simple CAC motif that defines the RSS cleavage-site and shows orientation-dependence best explained by a two-dimensional tracking mechanism. Deletion of the CBE-based IGCR1 IgH regulatory element disrupts antibody IgH recombination domains and, correspondingly, alters distributions of RAG on- and off-targets across the IgH locus. RAG off-targets frequently involved in chromosomal translocations occur in convergent RSS pairs at enhancer regions within a loop. Our findings reveal how RAG is developmentally focused and re-focused in lymphocytes and implicate mechanisms by which chromatin domains harness biological processes within them. We performed high-throughput genome-wide translocation sequencing (HTGTS) in progenitor B cells or cell lines to study signatures of RAG on and off-targeting activity using RAG-generated breaks in endogenous or ectopically-inserted paired bona fide RSSs as bait. Sequenceing was dong by Illumina Miseq.

2015-09-15 | E-GEOD-73007 | biostudies-arrayexpress

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Project description:Gene activation by Rag-mediated DNA double strand breaks

| PRJNA102521 | ENA

On-target and Off-target Activities of RAG Are Restricted by Topological Chromatin Domains

2015-09-15 | GSE73007 | GEO

BCLAF1 Chip-chip control (siGFP) and BRCA1 depleted (siBRCA1) 293T cells in the absense or presense of Etoposide

Project description:BCLAF1 is a serine-arginine (SR) protein implicated in transcriptional regulation and mRNA splicing. We have recently identified BCLAF1 as part of a novel mRNA splicing complex that is recruited to different genetic promoters by the breast cancer susceptiblity protein, BRCA1 in response to DNA damage. This ChIP-chip study was designed to identify genes/promoters regulated by the BRCA1/BCLAG1 mRNA splicing complex by identifying promoters bound by BCLAF1 in the absense and presense of BRCA1 in control cells and cells treated with etoposide to induce DNA damage. This study includes tripicate BCLAF1 ChIP-chip experiments in untreated and etoposide treated (1uM 16 hours) control cells (siGFP) and cells depleted of BRCA1 (siBRCA1). Chromatin Immunoprecipitaitons were performed in triplicate with BCLAF1 antibodies in control 293T cells transfected with siGFP siRNAs and BRCA1 siRNAs (siBRCA1 to deplete BRCA1). Immunoprecipitated genomic DNA was labelled with Cy3 and Input genomic DNA was labelled with Cy5 and hybridized to NimbleGen human 3x720k RefSeq promoter arrays to identify BCLAF1 boundgenomic DNA regions.

2014-04-25 | E-GEOD-47016 | biostudies-arrayexpress

BCLAF1 restrains stress responses in hematopoietic stem cells to support expansion and repopulation [RNA-seq]

Project description:Hematopoietic stem cells (HSC) rapidly expand during fetal development and after stress. Here, we identify BCLAF1 as a regulator of HSC repopulation activity with functions in propagation of fetal HSCs and hematopoietic reconstitution after stem cell transplantation. Using mice with hematopoietic-specific and inducible deletion of Bclaf1, we find that BCLAF1 promotes fetal HSC expansion but is dispensible for maintenance of adult HSCs at steady state. Loss of BCLAF1 in either fetal or adult HSCs significantly impairs their self-renewal and multi-lineage reconstitution activity after stem cell transplantation. Single-cell RNA sequencing of fetal hematopoietic progenitors reveals that loss of BCLAF1 reduces long-term HSCs and restrains expression of stress response genes. BCLAF1 associates with chromatin throughout the genome of fetal and adult hematopoietic cells, likely through indirect mechanisms, to regulate transcriptional programs. These results establish a novel function for the transcriptional regulator BCLAF1 in limiting stress responses in HSCs to preserve their expansion during embryogenesis and after stem cell transplant.

2025-08-20 | GSE279224 | GEO

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