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Distinct requirements of CHD4 during B cell development and antibody response

ABSTRACT: Distinct requirements of CHD4 during B cell development and antibody response

PROVIDER: PRJNA527119 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8730330_1.fastq.gz	Fastqsanger.gz
	SRR8730330_2.fastq.gz	Fastqsanger.gz
	SRR8730331_1.fastq.gz	Fastqsanger.gz
	SRR8730331_2.fastq.gz	Fastqsanger.gz
	SRR8730332_1.fastq.gz	Fastqsanger.gz

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Distinct requirements of CHD4 during B cell development and antibody response

Project description:Immunoglobulin heavy chain (Igh) class switch recombination (CSR) requires B cell proliferation, germline transcription, AID-instigated generation of DNA double strand breaks and DNA end-joining. How these various DNA-protein interactions and DNA transactions at Igh occur within the context of the chromatin landscape are largely unknown. Histone post-translational modifications can modulate chromatin accessibility and one such epigenetic mark, H3K9me3 is present at activated Igh switch sequences that serve as recombination targets during CSR. The chromatin remodeling protein CHD4 binds H3K9me3 and shapes chromatin accessibility and gene expression in various cell types, but its role in B cell biology is yet to be elucidated. Here, we conditionally ablated CHD4 expression in different stages of B cell development. We find that while CHD4 is essential for early B cell development, it is dispensable for homeostatic maintenance of mature naïve B cells and differentiation into antigen-specific early memory B cells and plasmablasts. However, loss of CHD4 in activated B cells leads to a severe defect in CSR, accompanied by markedly impaired cellular proliferation. Conditional deletion of p53 rescued the proliferation defect but failed to restore CSR due to a failure of AID to be efficiently recruited to Igh. This work unmasks a context-dependent role of CHD4 in B cell development and identifies CHD4 as a novel effector of CSR that influences B cell proliferation and recruitment of AID to Igh.

2019-05-29 | GSE128321 | GEO

Distinct Requirements of CHD4 during B Cell Development and Antibody Response.

Project description:The immunoglobulin heavy chain (Igh) locus features a dynamic chromatin landscape to promote class switch recombination (CSR), yet the mechanisms that regulate this landscape remain poorly understood. CHD4, a component of the chromatin remodeling NuRD complex, directly binds H3K9me3, an epigenetic mark present at the Igh locus during CSR. We find that CHD4 is essential for early B cell development but is dispensable for the homeostatic maintenance of mature, naive B cells. However, loss of CHD4 in mature B cells impairs CSR because of suboptimal targeting of AID to the Igh locus. Additionally, we find that CHD4 represses p53 expression to promote B cell proliferation. This work reveals distinct roles for CHD4 in B cell development and CSR and links the H3K9me3 epigenetic mark with AID recruitment to the Igh locus.

| S-EPMC6527137 | biostudies-literature

Distinct Notch1 and BCL11B requirements mediate human γδ/αβ T cell development

Project description:Distinct Notch1 and BCL11B requirements mediate human γδ/αβ T cell development

| PRJNA533059 | ENA

Distinct Notch1 and BCL11B requirements mediate human γδ/αβ T cell development [BCL11B_coculture]

Project description:Distinct Notch1 and BCL11B requirements mediate human γδ/αβ T cell development [BCL11B_coculture]

| PRJNA533188 | ENA

CHD4 and the NuRD complex directly control cardiac sarcomere formation

Project description:Cardiac development relies on proper cardiomyocyte differentiation including expression and assembly of cell-type specific actomyosin subunits into a functional cardiac sarcomere. Control of this process involves not only promoting expression of cardiac sarcomere subunits but also repressing expression of non-cardiac myofibril paralogs. This level of transcriptional control requires broadly expressed multiprotein machines that modify and remodel the chromatin landscape to restrict transcription machinery access. Prominent among these is the Nucleosome Remodeling and Deacetylase (NuRD) complex, which includes the catalytic core subunit CHD4. Here, we demonstrate that direct CHD4-mediated repression of skeletal and smooth muscle myofibril isoforms is required for normal cardiac sarcomere formation, function, and embryonic survival early in gestation. Through transcriptomic and system genome-wide analyses of CHD4 localization, we identified novel CHD4 binding sites in smooth muscle myosin heavy chain, fast skeletal α-actin, and the fast skeletal troponin complex genes. We further demonstrate that in the absence of CHD4, cardiomyocytes in the developing heart form a hybrid muscle cell that contains cardiac, skeletal and smooth muscle myofibril components. These misexpressed paralogs intercalate into the nascent cardiac sarcomere to disrupt sarcomere formation and cause impaired cardiac function in utero. These results demonstrate the genomic and physiological requirements for CHD4 in mammalian cardiac development.

2018-05-15 | GSE109012 | GEO

Distinct Notch1 and BCL11B requirements mediate human γδ/αβ T cell development [BCL11B_ex vivo]

Project description:Distinct Notch1 and BCL11B requirements mediate human γδ/αβ T cell development [BCL11B_ex vivo]

| PRJNA533187 | ENA

Distinct Notch1 and BCL11B requirements mediate human γδ/αβ T cell development [miRNA BCL11B_coculture]

Project description:Distinct Notch1 and BCL11B requirements mediate human γδ/αβ T cell development [miRNA BCL11B_coculture]

| PRJNA533190 | ENA

ZFHX4 and CHD4 ChIP sequencing in glioblastoma tumor initiating cells

Project description:Glioblastomas (GBM) harbor subpopulations of therapy-resistant tumor initiating cells (TICs) that are self-renewing and multipotent. To understand the regulation of the TIC state, we performed an image-based screen for genes regulating GBM TIC maintenance and identified ZFHX4, a 397-kDa transcription factor. ZFHX4 is required to maintain TIC-associated phenotypes in vitro, suggesting that ZFHX4 regulates TIC differentiation, and its suppression increases glioma-free survival in intracranial xenografts. ZFHX4 interacts with CHD4, a core member of the NuRD (nucleosome remodeling and deacetylase) complex. ZFHX4 and CHD4 bind to overlapping sets of genomic loci and control similar gene expression programs. Using expression data derived from GBM patients, we demonstrate ZFHX4 is a master regulator of CHD4-mediated gene expression. These observations define ZFHX4 as a regulatory factor that links the chromatin remodeling NuRD complex and the GBM TIC state. Examination of binding of ZFHX4 and CHD4 across the human genome, using the 0308 tumor initiating cell line. Two replicates for each protein, compared to whole cell extract inputs.

2014-01-16 | E-GEOD-52419 | biostudies-arrayexpress

Distinct Metabolic Requirements Regulate B Cell Activation and Germinal Center Responses

Project description:Distinct Metabolic Requirements Regulate B Cell Activation and Germinal Center Responses

| PRJNA973107 | ENA

Expression data from glioblastoma cells after ZFHX4 or CHD4 suppression.

Project description:ZFHX4 and CHD4 suppression independently shift tumor initiating cells out of a stem like state and toward a differentiated morphology. After gene suppression via transduction of a lentivirally mediated shRNA construct, RNA was extracted 3 and 5 days later and was hybridized on Affymetrix microarrays. Total RNA was extracted 3 and 5 days after shRNA transduction of 0308 TICs, for 3 (for CHD4) or 5 (ZFHX4) independent experiments. Complementary RNA synthesis and hybridization/scanning of U133 plus 2.0 microarrays using GeneChip products (Affymetrix) was done as described in the GeneChip manual.

2014-01-16 | E-GEOD-52363 | biostudies-arrayexpress

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