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The BCL6 RD2 domain governs commitment of activated B-cells to form germinal centers

ABSTRACT: Our data demonstrated that Bcl6 directly binds and represses trafficking receptors S1pr1 and Grp183 by recruiting Hdac2 through the RD2 domain. Deregulation of these genes impairs B-cell migration and may contribute to the Germinal Center failure in Bcl6RD2MUT mice. RNAseq was performed in endogenous BCL6-depleted OCI-LY1 cells rescued with either WT or RD mutant BCL6 (N=3 for each group).

ORGANISM(S): Homo sapiens

SUBMITTER: Yanwen Jiang

PROVIDER: E-GEOD-58365 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The BCL6 RD2 domain governs commitment of activated B cells to form germinal centers.

Huang Chuanxin C Gonzalez David G DG Cote Christine M CM Jiang Yanwen Y Hatzi Katerina K Teater Matt M Dai Kezhi K Hla Timothy T Haberman Ann M AM Melnick Ari A

Cell reports 20140828 5

To understand how the Bcl6 transcriptional repressor functions in the immune system, we disrupted its RD2 repression domain in mice. Bcl6RD2(MUT) mice exhibit a complete loss of germinal center (GC) formation but retain normal extrafollicular responses. Bcl6RD2(MUT) antigen-engaged B cells migrate to the interfollicular zone and interact with cognate T helper cells. However, these cells fail to complete early GC-commitment differentiation and coalesce as nascent GC aggregates. Bcl6 directly bind ...[more]

PMID: 25176650

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The BCL6 RD2 domain governs commitment of activated B-cells to form germinal centers

Project description:Our data demonstrated that Bcl6 directly binds and represses trafficking receptors S1pr1 and Grp183 by recruiting Hdac2 through the RD2 domain. Deregulation of these genes impairs B-cell migration and may contribute to the Germinal Center failure in Bcl6RD2MUT mice.

2014-09-14 | GSE58365 | GEO

Transcription profiling of chicken Bcl6 deficient DT40 B cell line to investigate the targets of Bcl6 which is required for germinal center formation

Project description:The transcription factor Bcl6 is required for germinal center formation and deregulated expression of Bcl6 has been observed in lymphomas. To gain insight to the function of Bcl6 in terminal differentiation of B cells to plasma cells and to investigate the targets of Bcl6, we established a Bcl6 deficient DT40 B cell line.

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Bcl6 expression specifies the T follicular helper cell program in vivo

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2012-09-17 | E-GEOD-40068 | biostudies-arrayexpress

Genome wide binding of BCL6 and LSD1 In GC derived lymphoma B cells

Project description:Using ChIP-seq we identified the genome wide targets of BCL6 and LSD1 in lymhpoma cells (OCI-Ly1) with control siRNA or siRNA targeted to BCL6

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BCL6 is required for the initiation and maintenance of chronic myeloid leukemia

Project description:We identified the BCL6 protooncogene as a critical downstream effector of FoxO3A in self-renewal signaling of CML-initiating cells. BCL6 represses Arf and p53 in CML cells and is required for leukemia stem cell maintenance, colony formation and initiation of leukemia in transplant recipients. Importantly, peptide inhibition of BCL6 in human CML cells compromises colony formation and leukemia-initiation in xenotransplanted mouse recipients. These findings identify peptide-inhibition of BCL6 as a novel strategy to eradicate leukemia-initiating cells in CML. Identification of BCL6 binding sites in human CML cell line JURL-MK1

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BCL6 ChIP on chip using a Nimblegen custom tiling array

Project description:To determine whether BCL6 binds to the certain locus we performed genomic localization studies by chromatin immunoprecipitations (ChIP) using a densely tiled custom oligonucleotide microarray covering the genomic loci of different genes. Keywords: ChIP-chip, Transcription Factor localization The experiment was performed in Ramos cell. Triplicate ChIP with BCL6 or actin (negative control) antibodies were cohybridized to the arrays versus the respective input chromatin.The fold enrichment for each oligonucleotide was calculated as the ratio of Cy5 vs. Cy3. Any peaks involving >5 oligonucleotides and with > 2.5 fold enrichment were considered potentially positive hits.

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2011-02-15 | E-GEOD-24404 | biostudies-arrayexpress

BCL6 enables leukemia cells to cope with inhibition of oncogenic tyrosine kinases

Project description:This SuperSeries is composed of the following subset Series: GSE24381: Inhibition of BCL6-dependent gene expression in Philadelphia chromosome positive acute lymphoblastic leukemia GSE24404: Recruitment of BCL6 to target genes in Philadelphia chromosome positive acute lymphoblastic leukemia Refer to individual Series

2011-02-15 | E-GEOD-24426 | biostudies-arrayexpress

ChIP-on-chip of BCL6

Project description:Identification BCL6 target genes in primary germinal center cells and DLBCL cell lines by ChIP-on-chip Three replicates in each type of cells

2010-06-21 | E-GEOD-15179 | biostudies-arrayexpress

Transcription factor Achaete-Scute homologue 2 initiates T follicular helper cell development [ChIP-Seq]

Project description:In immune responses, activated T cells migrate to B cell follicles and develop to T follicular helper (Tfh) cells, a new subset of CD4+ T cells specialized in providing help to B lymphocytes in the induction of germinal centers 1-3. Although Bcl6 has been shown to be essential in Tfh cell function, it may not regulate the initial migration of T cells 4 or the induction of Tfh program as exampled by CXCR5 upregulation 5. Here, we show that the Achaete-Scute homologue 2 (Ascl2) gene that encodes a basic helix-loop-helix (bHLH) transcription factor 6, is selectively upregulated in its expression in Tfh cells. Ectopic expression of Ascl2 uniquely upregulates CXCR5 but not Bcl6 and downregulates CCR7 expression in T cells in vitro and accelerates T cell migration to the follicles and Tfh cell development in vivo. Combined transcriptome profiling and genome-wide occupancy analysis indicate that Ascl2 directly regulates Tfh-related genes while inhibits expression of Th1 and Th17 genes. Acute deletion of Ascl2 as well as blockade of its function with the Id3 protein in peripheral CD4+ T cells results in a failure in Tfh cell development and the germinal center response. Conversely, mutation of Id3, known to cause antibody-mediated autoimmunity, greatly enhances Tfh cell generation. Thus, Ascl2 critically and directly initiates Tfh cell development. Decide Ascl2 binding sites in CD4+ T cells

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