Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE122830 | GEO | 2019/04/17

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

The NuRD complex suppresses transcriptional noise during lineage commitment [RNA-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 | GSE122696 | 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

Profiling the target genes for LSD1, MTA1, MTA2, and MTA3 in MCF-7

Project description:Using ChIP-DSL technology from AVIVA SYSTEMS BIOLOGY to find out the whole genome targets for LSD1, MTA1, MTA2, and MTA3 We analyzed arrays using antibodies against LSD1, MTA1, MTA2, or MTA3 and negative control to acquire the enriched ratio of each gene.

2009-08-21 | E-GEOD-14260 | biostudies-arrayexpress

GATA3/G9A/MTA3 sequencing in non-treated MCF-7 cells

Project description:Transcription factor GATA3 is essential for the specification and maintenance of the luminal cell differentiation in the mammary gland, and its expression is progressively lost during luminal breast cancer progression. However, how loss-of-function of GATA3 contributes to the development of breast cancer is still poorly understood. Here, we report that GATA3 nucleates a transcription repression program composed of G9A and MTA3-, but not MTA1- or MTA2-, constituted NuRD complex. Genome-wide analysis of the GATA3/G9A/NuRD(MTA3) targets identified a cohort of genes that are critically involved in epithelial-to-mesenchymal transition and cell invasion.

2015-03-25 | GSE67206 | GEO

Profiling the target genes for LSD1, MTA1, MTA2, and MTA3 in MCF-7

Project description:Using ChIP-DSL technology from AVIVA SYSTEMS BIOLOGY to find out the whole genome targets for LSD1, MTA1, MTA2, and MTA3

2009-08-21 | GSE14260 | GEO

The long non-coding RNA LINC00941 regulates human epidermal homeostasis through interaction with the MTA2/NuRD complex

Project description:Numerous long non-coding RNAs (lncRNAs) were shown to have functional impact on cellular processes, such as human epidermal homeostasis, but for only a few the mode of action has been elucidated. Here, we report that lncRNA LINC00941 controls keratinocyte differentiation on a global level through association with the MTA2/NuRD complex, one of the major chromatin remodelers in cells. LINC00941 was found to interact with NuRD-associated MTA2, suppressing the expression of the transcription factor EGR3, a regulator of epidermal differentiation. Both, LINC00941 and the MTA2/NuRD complex are enriched in non-differentiated keratinocytes and repress the expression of differentiation genes through epigenetic silencing of EGR3, consequentially repressing premature differentiation of human progenitor cells.

2024-04-08 | GSE237175 | GEO

The long non-coding RNA LINC00941 modulates MTA2/NuRD occupancy to suppress premature human epidermal differentiation

Project description:Numerous long non-coding RNAs (lncRNAs) were shown to have functional impact on cellular processes, such as human epidermal homeostasis, but for only a few the mode of action has been elucidated. Here, we report that lncRNA LINC00941 controls keratinocyte differentiation on a global level through association with the MTA2/NuRD complex, one of the major chromatin remodelers in cells. LINC00941 was found to interact with NuRD-associated MTA2, suppressing the expression of the transcription factor EGR3, a regulator of epidermal differentiation. Both LINC00941 and the MTA2/NuRD complex are enriched in non-differentiated keratinocytes and repress the expression of differentiation genes through epigenetic silencing of EGR3, consequentially preventing premature differentiation of human progenitor cells.

2024-04-08 | PXD043838 | Pride

Zic2, an enhancer-binding factor required for embryonic stem cell specification

Project description:The Zinc finger protein of the cerebellum 2 (Zic2) is one of the vertebrate homologs of the Drosophila pair-rule gene odd-paired (opa). Our molecular and biochemical studies have demonstrated that Zic2 to preferentially bind to transcriptional enhancers and functions as a cofactor that interacts with the NuRD complex in ES cells. Detailed genome-wide studies demonstrate that Zic2 function with Mbd3/NuRD in regulating the chromatin state and transcriptional output of genes linked to differentiation. Zic2 is dispensable for the selfrenewal of ES cells but is required for proper differentiation, similar to what has been previously reported for Mbd3/NuRD. Our study identifies Zic2 as a key factor in the execution of the pluripotency program with Mbd3/NuRD in ES cells. ChIP-seq of Zic2, Chd4, Mbd3 and Zic3 in mES cells. ChIP-seq of H3K27me3, H3K27ac, H3K4me3, H3K4me1 and PolII in mES cells after Zic2 shRNA and non-targeting shRNA. RNA-seq of mES cells after Zic2, Zic3, Mbd3 and Mta2 shRNA and non-targeting shRNA.

2015-02-23 | E-GEOD-61188 | biostudies-arrayexpress

MUC1-C ACTIVATES THE NURD COMPLEX IN DEDIFFERENTIATION OF TRIPLE-NEGATIVE BREASTCANCER CELLS

Project description:The NuRD chromatin remodeling and deacetylation complex, which includes MTA1, MBD3, CHD4 and HDAC1 among other components, is of importance for development and cancer progression. The oncogenic MUC1-C protein activates EZH2 and BMI1 in the epigenetic reprogramming of triple-negative breast cancer (TNBC) cells. However, there is no known link between MUC1-C and chromatin remodeling complexes. The present studies demonstrate that MUC1-C binds directly to the MYC HLH/LZ domain. In turn, we identified a previously unrecognized MUC1-C®MYC pathway that regulates the NuRD complex. We show that MUC1-C/MYC complexes selectively activate the MTA1 and MBD3 genes and posttranscriptionally induce CHD4 expression in basal- and not luminal-type BC cells. The results further show that MUC1-C forms complexes with these NuRD components on the ESR1 promoter. In this way, silencing MUC1-C (i) decreased MTA1/MBD3/CHD4/HDAC1 occupancy and increased H3K27 acetylation on the ESR1 promoter, and (ii) induced ESR1 expression and downstream estrogen response pathways. We also demonstrate that targeting MUC1-C and these NuRD components induces expression of FOXA1, GATA3 and other markers associated with the luminal phenotype. These findings and results from gain-of-function studies support a model in which MUC1-C activates the NuRD complex in driving luminal®basal dedifferentiation and plasticity of TNBC cells.

2020-03-05 | GSE134147 | GEO