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CHD4 is essential for transcriptional repression and lineage progression in B lymphopoiesis

ABSTRACT: CHD4 is essential for transcriptional repression and lineage progression in B lymphopoiesis

PROVIDER: PRJNA508953 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8308140.fastq.gz	Fastqsanger.gz
	SRR8308150_1.fastq.gz	Fastqsanger.gz
	SRR8308150_2.fastq.gz	Fastqsanger.gz
	SRR8308141.fastq.gz	Fastqsanger.gz
	SRR8308151_1.fastq.gz	Fastqsanger.gz

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CHD4 is essential for transcriptional repression and lineage progression in B lymphopoiesis [RNA-seq]

Project description:Cell-lineage specification is a tightly regulated process that is dependent on appropriate expression of lineage- and developmental stage-specific transcriptional programs. Accessibility and inaccessibility of gene loci are controlled dynamically during cellular development. Here, we show that Chromodomain Helicase DNA-binding protein 4 (CHD4), a major ATPase/helicase subunit of Nucleosome Remodeling and Deacetylase Complexes (NuRD) in lymphocytes, is essential for specification of the early B cell lineage transcriptional program. In the absence of CHD4 in early B cell progenitors in vivo, B cell progenitors are arrested at an early pro-B-like stage of development, unresponsive to IL-7 receptor signaling and complete V(D)J rearrangements at Igh loci inefficiently. Importantly, CHD4-deficient B cells express a significant number of non-B cell lineage genes, including genes involved in the development of other hematopoietic lineages and neuronal cells. The absence of CHD4 increased chromatin accessibility at hundreds of these gene loci, suggesting that its ability to repress transcription by mobilizing nucleosomes and compacting chromatin is a barrier against inappropriate transcription. Together, our data demonstrate the importance of CHD4 in establishing and maintaining an appropriate transcriptome in early B lymphopoiesis via chromatin accessibility.

2019-04-30 | GSE123502 | GEO

CHD4 is essential for transcriptional repression and lineage progression in B lymphopoiesis [ATAC-seq]

2019-04-30 | GSE123503 | GEO

CHD4 is essential for transcriptional repression and lineage progression in B lymphopoiesis [ATAC-seq]

Project description:CHD4 is essential for transcriptional repression and lineage progression in B lymphopoiesis [ATAC-seq]

| PRJNA508955 | ENA

CHD4 is essential for transcriptional repression and lineage progression in B lymphopoiesis [RNA-seq]

Project description:CHD4 is essential for transcriptional repression and lineage progression in B lymphopoiesis [RNA-seq]

| PRJNA508956 | ENA

CHD4 is essential for transcriptional repression and lineage progression in B lymphopoiesis.

Project description:Cell lineage specification is a tightly regulated process that is dependent on appropriate expression of lineage and developmental stage-specific transcriptional programs. Here, we show that Chromodomain Helicase DNA-binding protein 4 (CHD4), a major ATPase/helicase subunit of Nucleosome Remodeling and Deacetylase Complexes (NuRD) in lymphocytes, is essential for specification of the early B cell lineage transcriptional program. In the absence of CHD4 in B cell progenitors in vivo, development of these cells is arrested at an early pro-B-like stage that is unresponsive to IL-7 receptor signaling and unable to efficiently complete V(D)J rearrangements at Igh loci. Our studies confirm that chromatin accessibility and transcription of thousands of gene loci are controlled dynamically by CHD4 during early B cell development. Strikingly, CHD4-deficient pro-B cells express transcripts of many non-B cell lineage genes, including genes that are characteristic of other hematopoietic lineages, neuronal cells, and the CNS, lung, pancreas, and other cell types. We conclude that CHD4 inhibits inappropriate transcription in pro-B cells. Together, our data demonstrate the importance of CHD4 in establishing and maintaining an appropriate transcriptome in early B lymphopoiesis via chromatin accessibility.

| S-EPMC6561196 | biostudies-literature

CHD4 is essential for transcriptional repression and lineage progression in B lymphopoiesis

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-04-29 | GSE123504 | GEO

Chromodomain Helicase DNA-binding 4 (CHD4) is required for B cell identity and lineage progression

Project description:B cell specification and identity are controlled by transcription factors and cytokine receptors that drive the expression of stage-specific transcriptomes during lineage progression. A key feature of these mechanisms is the repression of inappropriate transcription. Here, we utilized RNA-seq to demonstrate that chromodomain helicase DNA-binding protein 4 (CHD4), an ATPase/helicase subunit of Mi-2/NuRD chromatin remodeling complexes, is essential for B cell identity. In mice that lack CHD4 selectively in the B lineage, defects include developmental arrest at the early pro-B cell stage. While many pro-B-specific genes are expressed in the mutant cells, transcripts that are normally restricted to other tissues including pancreas and bone are expressed out of context. Moreover, CHD4-deficient pro-B cells do not proliferate in response to IL-7, exhibit greatly decreased utilization of distal VH segments and accumulate DNA damage. Together, our data confirm the importance of CHD4 and NuRD complexes for the generation of functional B cells.

2019-05-22 | GSE84806 | GEO

Chd4 ensures stem cell lineage fidelity during skeletal muscle regeneration

Project description:The chromatin remodeler Chd4, a member of the nucleosome remodeling and deacetylase (NuRD) repressive complex, is essential for the expansion and regenerative functions of satellite cells.

2021-09-03 | GSE179683 | GEO

CHD4 regulates super-enhancer accessibility in fusion-positive rhabdomyosarcoma and is essential for tumor growth

Project description:ATP-dependent chromatin remodelers modulate gene expression by regulating genome accessibility and can contribute to tumorigenesis. In fusion-positive rhabdomyosarcoma (FP-RMS), we have previously identified the chromatin remodeler and NuRD subunit CHD4 as an essential gene for tumor survival. Here, we demonstrate that the FP-RMS vulnerability to CHD4 goes beyond its function as a NuRD member. Mechanistically, CHD4 interacts with BRD4 and co-localizes with the tumor driver and fusion protein PAX3-FOXO1 at super-enhancers where it generates a chromatin architecture permissive for the binding of the fusion protein. This allows the positioning of RNA polymerase 2 at promoters and the expression of the oncogenic program of PAX3-FOXO1. Additionally, analysis of genome-wide cancer dependency databases identifies CHD4 amongst the NuRD subunits as general novel cancer vulnerability. Our findings describe, for the first time, CHD4 as a regulator of super-enhancer-mediated gene expression and establish this chromatin remodeler as an unexpected broad tumor susceptibility.

2019-12-20 | GSE140115 | GEO

Chd4 deficiency effect on mouse embryonic stem cells

Project description:Our study reveal that Chd4 is essential for stemness maintenance of ESCs. As Chd4 deficient ESCs show attentuated self-renewal ability and induced differentiation marker gene expression. To confirm the effect of Chd4 on the transcriptome profile of ESCs, we performed microarray analyses for Chd4 deficient ESCs.

2017-05-01 | GSE89675 | GEO

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