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The NuRD complex suppresses transcriptional noise during lineage commitment

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

ORGANISM(S): Mus musculus

PROVIDER: GSE122833 | GEO | 2019/04/17

REPOSITORIES: GEO

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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 [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 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

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

| PRJNA506448 | ENA

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

Transcriptional heterogeneity and lineage commitment in myeloid progenitors

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-11-25 | E-GEOD-72859 | biostudies-arrayexpress

Transcriptional diversity during lineage commitment of human blood progenitors.

Project description:Blood cells derive from hematopoietic stem cells through stepwise fating events. To characterize gene expression programs driving lineage choice, we sequenced RNA from eight primary human hematopoietic progenitor populations representing the major myeloid commitment stages and the main lymphoid stage. We identified extensive cell type-specific expression changes: 6711 genes and 10,724 transcripts, enriched in non-protein-coding elements at early stages of differentiation. In addition, we found 7881 novel splice junctions and 2301 differentially used alternative splicing events, enriched in genes involved in regulatory processes. We demonstrated experimentally cell-specific isoform usage, identifying nuclear factor I/B (NFIB) as a regulator of megakaryocyte maturation-the platelet precursor. Our data highlight the complexity of fating events in closely related progenitor populations, the understanding of which is essential for the advancement of transplantation and regenerative medicine.

| S-EPMC4254742 | biostudies-literature

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