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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE123504 | GEO | 2019/04/29

REPOSITORIES: GEO

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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 [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.

2019-04-30 | GSE123503 | GEO

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

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

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

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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]

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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]

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ZEB1 controls a lineage-specific transcriptional program essential for melanoma cell state transitions

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