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

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

PROVIDER: PRJNA530207 | ENA |

REPOSITORIES: ENA

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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]

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Gene activation by Rag-mediated DNA double strand breaks

Project description:The objective is to identify genes that are differentially expressed following the introduction of DNA double strand breaks (DSBs) by the Rag proteins in murine pre-B cells. Cells lacking Artemis are used since the Rag-induced DSBs will not be repaired and, thus, will provide a continuous stimulus to the cell. Cells lacking Artemis and Atm are used to determine which gene expression changes depend on Atm and cells lacking Artemis that express an I kappa B alpha dominant negative are used to determine which gene expression changes depend on NFkB.

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RAG-Mediated DNA Breaks Attenuate PU.1 Activity in Early B Cells through Activation of a SPIC-BCLAF1 Complex.

Project description: Not available

| S-EPMC6870970 | biostudies-literature

Gene activation by Rag-mediated DNA double-strand breaks in G1-phase murine pre-B cells

Project description:The objective is to identify genes that are differentially expressed following the introduction of DNA double-strand breaks (DSBs) by the Rag proteins in murine pre-B cells. Cells lacking Artemis are used since the Rag-induced DSBs will not be repaired, and thus, will provide a continuous stimulus to the cell. Murine v-abl-transformed pre-B cells were treated with 3 uM STI571 for 48 hours. Cell types included RAG-2-deficient (3 biological replicates) and Artemis-deficient (3 biological replicates) G1-phase pre-B cells. Each sample was hybridized once using Affymetrix Mouse Genome 2.0 GeneChip arrays (Mouse 430 v2, Affymetrix, Santa Clara, CA). Data were analyzed using the RAG-2-deficient samples as the controls.

2013-03-13 | E-GEOD-38044 | biostudies-arrayexpress

Gene activation by Rag-mediated DNA double-strand breaks in G1-phase murine pre-B cells

2013-03-13 | GSE38044 | GEO

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

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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

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

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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