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The NuRD complex suppresses transcriptional noise during lineage commitment [ChIP-Seq]

ABSTRACT: The NuRD complex suppresses transcriptional noise during lineage commitment [ChIP-Seq]

PROVIDER: PRJNA506448 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8236020.fastq.gz	Fastqsanger.gz
	SRR8236030.fastq.gz	Fastqsanger.gz
	SRR8236021.fastq.gz	Fastqsanger.gz
	SRR8236031.fastq.gz	Fastqsanger.gz
	SRR8236022.fastq.gz	Fastqsanger.gz

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The NuRD complex suppresses transcriptional noise during lineage commitment

Project description:The NuRD complex suppresses transcriptional noise during lineage commitment

| PRJNA506450 | ENA

The NuRD complex suppresses transcriptional noise during lineage commitment [RNA-Seq]

Project description:The NuRD complex suppresses transcriptional noise during lineage commitment [RNA-Seq]

| PRJNA506028 | ENA

The NuRD complex suppresses transcriptional noise during lineage commitment [ChIP-Seq]

Project description:Here we set out to define the biochemical and functional diversity encoded by one such group of proteins within the mammalian Nucleosome Remodelling and Deacetylation (NuRD) complex: Mta1, Mta2 and Mta3. We find that, in contrast to what has been described in somatic cells, MTA proteins are not mutually exclusive within ES cell NuRD and, despite subtle differences in chromatin binding and biochemical interactions, serve largely redundant functions. ES cells lacking all three MTA proteins represent a complete NuRD null and are viable, allowing us to identify a highly previously unreported function for NuRD in reducing transcriptional noise, which is essential for maintaining a proper differentiation trajectory during early stages of lineage commitment.

2019-04-17 | GSE122830 | GEO

The NuRD complex suppresses transcriptional noise during lineage commitment [RNA-Seq]

2019-04-17 | GSE122696 | GEO

The NuRD complex suppresses transcriptional noise during lineage commitment

Project description:Multiprotein chromatin remodelling complexes show remarkable conservation of function amongst metazoans, even though components present in invertebrates are often found as multiple paralogous proteins in vertebrate complexes. In some cases these paralogues specify distinct biochemical and/or functional activities in vertebrate cells. Here we set out to define the biochemical and functional diversity encoded by one such group of proteins within the mammalian Nucleosome Remodelling and Deacetylation (NuRD) complex: Mta1, Mta2 and Mta3. We find that, in contrast to what has been described in somatic cells, MTA proteins are not mutually exclusive within ES cell NuRD and, despite subtle differences in chromatin binding and biochemical interactions, serve largely redundant functions. ES cells lacking all three MTA proteins exhibit complete NuRD loss-of-function and are viable, allowing us to identify a previously unreported function for NuRD in reducing transcriptional noise, which is essential for maintaining a proper differentiation trajectory during early stages of lineage commitment.

| S-SCDT-EMBOJ-2018-100788 | biostudies-other

The NuRD complex suppresses transcriptional noise during lineage commitment

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

2019-04-17 | GSE122833 | GEO

MTA proteins act redundantly within the NuRD complex to ensure fidelity of ES cell lineage commitment

Project description:Multiprotein chromatin remodelling complexes show remarkable conservation of function amongst metazoans, even though each component present in invertebrates are often present as multiple paralogous proteins in vertebrate complexes. In some cases these paralogues have been shown to specify distinct biochemical and/or functional activities in vertebrate cells. Here we set out to define the biochemical and functional diversity encoded by one such group of proteins within the mammalian Nucleosome Remodelling and Deaceylation (NuRD) complex: Mta1, Mta2 and Mta3. We find that, in contrast to what has been described in somatic cells, MTA proteins are not mutually exclusive within ES cell NuRD and, despite subtle differences in chromatin binding and biochemical interactions, serve largely redundant functions. Nevertheless, ES cells lacking all three MTA proteins represent a complete NuRD null and are viable, allowing us to identify a previously undetected function for NuRD in maintaining differentiation trajectory during early stages of lineage commitment.

2019-03-26 | PXD009855 | Pride

The Nucleosome Remodelling and Deacetylation complex suppresses transcriptional noise during lineage commitment.

Project description:Multiprotein chromatin remodelling complexes show remarkable conservation of function amongst metazoans, even though components present in invertebrates are often found as multiple paralogous proteins in vertebrate complexes. In some cases, these paralogues specify distinct biochemical and/or functional activities in vertebrate cells. Here, we set out to define the biochemical and functional diversity encoded by one such group of proteins within the mammalian Nucleosome Remodelling and Deacetylation (NuRD) complex: Mta1, Mta2 and Mta3. We find that, in contrast to what has been described in somatic cells, MTA proteins are not mutually exclusive within embryonic stem (ES) cell NuRD and, despite subtle differences in chromatin binding and biochemical interactions, serve largely redundant functions. ES cells lacking all three MTA proteins exhibit complete NuRD loss of function and are viable, allowing us to identify a previously unreported function for NuRD in reducing transcriptional noise, which is essential for maintaining a proper differentiation trajectory during early stages of lineage commitment.

| S-EPMC6576150 | biostudies-literature

NuRD suppresses pluripotency gene expression to promote transcriptional heterogeneity and lineage commitment.

Project description:Transcriptional heterogeneity within embryonic stem cell (ESC) populations has been suggested as a mechanism by which a seemingly homogeneous cell population can initiate differentiation into an array of different cell types. Chromatin remodeling proteins have been shown to control transcriptional variability in yeast and to be important for mammalian ESC lineage commitment. Here we show that the Nucleosome Remodeling and Deacetylation (NuRD) complex, which is required for ESC lineage commitment, modulates both transcriptional heterogeneity and the dynamic range of a set of pluripotency genes in ESCs. In self-renewing conditions, the influence of NuRD at these genes is balanced by the opposing action of self-renewal factors. Upon loss of self-renewal factors, the action of NuRD is sufficient to silence transcription of these pluripotency genes, allowing cells to exit self-renewal. We propose that modulation of transcription levels by NuRD is key to maintaining the differentiation responsiveness of pluripotent cells.

| S-EPMC3402183 | biostudies-literature

NuRD complex recruitment to Thpok mediates CD4+ T cell lineage differentiation

Project description:Although BTB-zinc finger (BTB-ZF) transcription factors control the differentiation of multiple hematopoietic and immune lineages, how they function is poorly understood. The BTB-ZF factor Thpok controls intrathymic CD4+ T cell development and expression of most CD4+- and CD8+-lineage genes. Here, we identify the nucleosome remodeling and deacetylase (NuRD) complex as a novel Thpok cofactor. We locate three amino-acid residues within the Thpok BTB domain that are required for both NuRD binding and Thpok functions, and show that NuRD recruitment recapitulates the functions of the Thpok BTB domain. NuRD mediates Thpok repression of CD8+-lineage genes, including the transcription factor Runx3, but is dispensable for Cd4 expression. We show that these functions cannot be performed by the BTB domain of the Thpok-related factor Bcl6, which fails to bind NuRD. Thus, cofactor binding critically contributes to the functional specificity of BTB-zinc finger factors, which control the differentiation of most hematopoietic subsets.

2022-06-10 | GSE199739 | GEO

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