Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

BCL6 ChIP on chip using a Nimblegen custom tiling array

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Jose Polo

PROVIDER: E-GEOD-7673 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Bcl-6 mediates the germinal center B cell phenotype and lymphomagenesis through transcriptional repression of the DNA-damage sensor ATR.

Ranuncolo Stella Maris SM Polo Jose M JM Dierov Jamil J Singer Michael M Kuo Tracy T Greally John J Green Roland R Carroll Martin M Melnick Ari A

Nature immunology 20070610 7

Antibody specificity and diversity is generated in B cells during germinal center maturation through clonal expansion while they undergo class-switch recombination and somatic hypermutation. Here we demonstrate that the transcriptional repressor Bcl-6 mediates this phenotype by directly repressing ATR in centroblasts and lymphoma cells. ATR is critical in replication and DNA damage-sensing checkpoints. Bcl-6 allowed B cells to evade ATR-mediated checkpoints and attenuated the response of the B c ...[more]

PMID: 17558410

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Project description:Linker histones are involved in the formation of higher-order chromatin structure. Although linker histones have been implicated in the regulation of specific genes, it still remains unclear what their principal binding determinants are and how their repressive function in vitro can be reconciled with presumed broad binding in vivo. We generated a full genome, high resolution binding map of linker histone H1 in Drosophila Kc cells, using DamID. H1 binds at similar levels across much of the genome, both in classical euchromatin and heterochromatin. Strikingly, there are pronounced dips of low H1 occupancy around transcription start sites of active genes and at many distant cis-regulatory sites. H1 dips are not due to lack of nucleosomes. Rather, all regions with low binding of H1 show enrichment of the histone variant H3.3 which itself has been linked to high nucleosome turnover. Upon knockdown of H3.3, we find that H1 levels increase at sites previously not covered with H1 with a concomitant increase in nucleosome repeat length. These changes are independent of transcriptional changes. Our results show that the H3.3 protein counteracts association of H1 at genomic sites with high rates of histone turnover. This antagonism provides a mechanism to keep diverse genomic sites in an open chromatin conformation. For this study, we generated DamID profiles of histone H1 and RpII18 in Drosophila Kc167 cells. Additionally, we generated H1 profiles in cells treated with RNAi against white, H3.3B, or H3.3A and H3.3B. Nucleosome positioning profiles were generated in untreated cells and cells treated with RNAi against white, H3.3B, or H3.3A and H3.3B. Profiles of expression changes were generated for H3.3B RNAi and H3.3A and H3.3B RNAi. DamID experiments for H1 and RpII18 were performed in Drosophila cell cultures. Samples were hybridized to 380k NimbleGen arrays with 300 bp probe spacing. Formaldehyde-assisted isolation of regulatotry elements (FAIRE) was performed in Drosophila Kc167 cells. Samples were hybridized to 380k NimbleGen arrays with 300 bp probe spacing over non-crosslinked genomic DNA. Nucleosome positioning profiles were made by hybridizing mononucleosomal DNA over MNase digested purified genomic DNA on 380k NimbleGen arrays with 10 bp probe spacing. Expression profiles were made as H3.3 RNAi over white RNAi cohybridizations on spotted INDAC long oligo arrays. Every experiment was done in duplicate in the reverse dye orientation.

Dataset Information

BCL6 ChIP on chip using a Nimblegen custom tiling array

Publications

Bcl-6 mediates the germinal center B cell phenotype and lymphomagenesis through transcriptional repression of the DNA-damage sensor ATR.

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