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Differential programming of B cells in Aicda-/- mice [MethylCap-Seq]

ABSTRACT: We determined CpG methylation load from GC B cells obtained from both Aicda-/- and Aicda+/+ mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE47704 | GEO | 2013/06/07

SECONDARY ACCESSION(S): PRJNA207340

REPOSITORIES: GEO

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Differential programming of B cells in Aicda-/- mice [MethylCap-Seq]

Project description:We determined CpG methylation load from GC B cells obtained from both Aicda-/- and Aicda+/+ mice. Examination of methylation load of Aicda-/- and Acida+/+ GC B cells.

2013-06-07 | E-GEOD-47704 | biostudies-arrayexpress

Differential programming of B cells in Aicda-/- mice [RNA-Seq]

Project description:We sequenced mRNA from naive, in vitro activated, and GC B cells obtained from both Aicda-/- and Aicda+/+ mice. Examination of mRNA levels in naive, in vitro activated, and GC B cells.

2013-06-07 | E-GEOD-47703 | biostudies-arrayexpress

Differential programming of B cells in Aicda-/- mice [RNA-Seq]

Project description:We sequenced mRNA from naive, in vitro activated, and GC B cells obtained from both Aicda-/- and Aicda+/+ mice.

2013-06-07 | GSE47703 | GEO

AICDA-induced epigenetic plasticity accelerates germinal center-derived lymphomagenesis

Project description:Epigenetic heterogeneity is emerging as a significant phenotypic feature of tumors. In diffuse large B-cell lymphomas (DLBCLs), increased cytosine methylation heterogeneity is associated with poor clinical outcome, yet the biological mechanisms driving epigenetic heterogeneity remain unclear. Activation-induced cytidine deaminase (AICDA), an enzyme that deaminates and facilitates demethylation of DNA methyl-cytosines in germinal center (GC) B-cells, is required for DLBCL pathogenesis and linked to inferior clinical outcomes. Here, we show that overexpression of AICDA causes more aggressive disease and worse outcome in BCL2-driven murine lymphomas. This phenotype was associated with significantly increased focal inter-tumor and intra-tumor cytosine methylation heterogeneity as compared to control lymphomas, but not with increased mutational burden. AICDA-mediated epigenetic heterogeneity was accompanied by DNA hypomethylation. Reciprocally, we observed that the focal inter-individual and intra-individual cytosine methylation heterogeneity characteristic of normal GC B-cells was lost upon depletion of AICDA. There was significant overlap of AICDA-induced methylation heterogeneity foci in GC B-cells and murine lymphomas. These observations are relevant to human patients, since DLBCLs with high AICDA expression likewise manifest extensive increases in focal inter-patient and intra-patient heterogeneity as compared to DLBCLs with low AICDA expression. Affected regions significantly overlapped with those found in murine AICDA-overexpressing lymphomas. Our results identify AICDA as a novel source of epigenetic plasticity and heterogeneity in B-cell lymphomas with potential significance for other tumors that express cytosine deaminases.

2018-01-19 | GSE95013 | GEO

Differential programming of B cells in Aicda-/- mice

Project description:Differential programming of B cells in Aicda-/- mice

| PRJNA207339 | ENA

Reduced Representation Bisulphite Sequencing of WT and AICDA KO iPCS clones

Project description:We report AICDA facilitates naïve pluripotency of mouse iPSCs by suppressing FGF/ERK signaling. In the absence of AICDA iPSCs fail to achive naïve pluripotent state and display chracteristics of EpiSCs and are primed for differentiation.

2019-04-03 | GSE129187 | GEO

SETD2 haploinsufficiency enhances germinal center-associated AICDA somatic hypermutation to drive B-cell lymphomagenesis

Project description:SETD2 is the sole chromatin modifier responsible for H3K36me3, a histone mark linked to splicing, transcription initiation and DNA damage response. Homozygous disruption of SETD2 yields a tumor suppressor effect in various cancers. However, SETD2 mutation is virtually always heterozygous in diffuse large B-cell lymphomas (DLBCL). Here we show that heterozygous SETD2 deficiency results in germinal center (GC) hyperplasia and accelerated lymphomagenesis. SETD2 haploinsufficient GC B-cells exhibit increased competitive fitness and reduced DNA damage checkpoint activity, resulting in decreased apoptosis. SETD2 haploinsufficient GCB and lymphoma cells featured increased off- and on-target AICDA induced somatic hypermutation (SHM), complex structural variants such as rygma, and increased translocations including those activating MYC. DNA damage was selectively increased on the non-template strand and H3K36me3 loss was associated with greater RNA Pol II processivity and mutational burden, suggesting that SETD2-mediated H3K36me3 is required for proper sensing of cytosine deamination during transcription. Hence, SETD2 haploinsufficiency delineates a novel GC B-cell context specific oncogenic pathway involving defective epigenetic surveillance of AICDA mediated somatic hypermutation induced off target effects on transcribed genes.

2022-04-06 | GSE189867 | GEO

RNA sequencing of WT and AICDA KO iPCS clones

2019-04-03 | GSE129186 | GEO

Differential programming of B cells in Aicda-/- mice

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-06-07 | E-GEOD-47705 | biostudies-arrayexpress

TET enzymes augment AID expression via 5hmC modifications at the Aicda superenhancer [BS-seq]

Project description:TET enzymes are dioxygenases that promote DNA demethylation by oxidizing the methyl group of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC). Here we report a close correspondence between 5hmC-marked regions, chromatin accessibility and enhancer activity in B cells, and a strong enrichment for consensus binding motifs for basic region-leucine zipper (bZIP) transcription factors at TET-responsive genomic regions. Functionally, Tet2 and Tet3 regulate class switch recombination (CSR) in murine B cells by enhancing expression of Aicda, encoding the cytidine deaminase AID essential for CSR. TET enzymes deposit 5hmC, demethylate and maintain chromatin accessibility at two TET-responsive elements, TetE1 and TetE2, located within a superenhancer in the Aicda locus. Transcriptional profiling identified BATF as the bZIP transcription factor involved in TET-dependent Aicda expression. 5hmC is not deposited at TetE1 in activated Batf-deficient B cells, indicating that BATF recruits TET proteins to the Aicda enhancer. Our data emphasize the importance of TET enzymes for bolstering AID expression, and highlight 5hmC as an epigenetic mark that captures enhancer dynamics during cell activation.

2019-04-29 | GSE116202 | GEO

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