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The Chd4 helicase regulates chromatin accessibility and gene expression critical for β-cell function in vivo [ATAC-seq]

ABSTRACT: The Chd4 helicase regulates chromatin accessibility and gene expression critical for β-cell function in vivo [ATAC-seq]

PROVIDER: PRJNA899040 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22215322_1.fastq.gz	Fastqsanger.gz
	SRR22215322_2.fastq.gz	Fastqsanger.gz
	SRR22215323_1.fastq.gz	Fastqsanger.gz
	SRR22215323_2.fastq.gz	Fastqsanger.gz
	SRR22215324_1.fastq.gz	Fastqsanger.gz

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The Chd4 helicase regulates chromatin accessibility and gene expression critical for β-cell function in vivo.

Project description:The Chd4 helicase regulates chromatin accessibility and gene expression critical for β-cell function in vivo.

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The Chd4 helicase regulates chromatin accessibility and gene expression critical for β-cell function in vivo [RNA-seq]

Project description:The Chd4 helicase regulates chromatin accessibility and gene expression critical for β-cell function in vivo [RNA-seq]

| PRJNA899041 | ENA

The Chd4 helicase regulates chromatin accessibility and gene expression critical for β-cell function in vivo [ATAC-seq]

Project description:To establish the role of Chd4 on controlling gene expression programs in the beta cell, we generated a tamoxifen-inducible, beta-cell-specific knockout mouse model; control (MIP-CreERT; Chd4flox/+;R26RtdTomato) and Chd4Db (MIP-CreERT; Chd4flox/flox;R26RtdTomato.

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The Chd4 helicase regulates chromatin accessibility and gene expression critical for β-cell function in vivo [RNA-seq]

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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 is essential for transcriptional repression and lineage progression in B lymphopoiesis [ATAC-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.

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

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The Chd4 helicase regulates chromatin accessibility and gene expression critical for β-cell function in vivo.

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

2023-05-31 | GSE217446 | GEO

CHD4 acts as a critical regulator in the survival of spermatogonial stem cells in mice [CUT&TAG]

Project description:Male spermatogenesis is sustained by homeostatic balance between the self-renewal and differentiation of spermatogonial stem cells (SSCs), which is dependent on the strict regulation of transcriptional factor and chromatin modulator gene expression. Chromodomain helicase DNA-binding protein 4 (CHD4) is highly expressed in SSCs but roles in mouse spermatogenesis are unexplored. Here, we report that the germ-cell-specific deletion of Chd4 resulted in complete infertility in male mice, with rapid loss of SSCs and excessive germ cell apoptosis. Chd4-knockdown in cultured SSCs also promoted the expression of apoptosis-related genes and thereby activated the tumor necrosis factor signaling pathway. Mechanistically, CHD4 occupies the genomic regulatory region of key apoptosis-related genes including Jun and Nfkb1. Together, our findings reveal the determinant role of CHD4 in SSCs survival in vivo, which will offer insight into the pathogenesis of male sterility and potential novel therapeutic targets.

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CHD4 acts as a critical regulator in the survival of spermatogonial stem cells in mice [RNA-Seq]

2022-01-08 | GSE193069 | GEO