ChIP-seq of NuRD components and pluripotency factors in wild-type, Mbd3 and Sall4/1 mutant embryonic stem cells
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PROVIDER: PRJEB13059 | ENA |
REPOSITORIES: ENA
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Project description:Members of the Nucleosome Remodeling and Deacetylase (NuRD) complex Mbd3 and Mi2beta (Chd4) along with pluripotency regulators Nanog, Oct4, Klf4 and Esrrb were profiled for chromatin association by ChIP-seq in mouse embryonic stem cells mutant for Mbd3, Sall4 and/or the related Sall1 pluripotency-associated factors.
2016-08-09 | E-MTAB-4565 | biostudies-arrayexpress
Project description:Sall4 is a transcription factor essential for early mammalian development. Though it is reported to play an important role in embryonic stem (ES) cell self-renewal, whether it is an essential pluripotency factor has been disputed. Though Sall4 is known to associate with the Nucleosome Remodeling and Deacetylase (NuRD) complex, the nature of this interaction is unclear as NuRD and Sall4 serve opposing functions in ES cells. Here we use defined culture conditions and single-cell gene expression analyses to show that Sall4 prevents activation of the neural gene expression programme in ES cells but is dispensable for maintaining the pluripotency gene regulatory network. We further show using genome-wide analyses that while Sall4 interacts with NuRD, it neither recruits NuRD to chromatin nor influences transcription via NuRD. Rather we propose a model where, by titrating Sall4 protein, NuRD limits the differentiation-inhibiting activity of Sall4 in ES cells to enable lineage commitment.
2016-08-02 | PXD003614 | Pride
Project description:To obtain a comprehensive and quantitative view on MBD2 vs MBD3-NuRD complex stoichiometry, we performed biotin co-immunoprecipitations in Mbd3 KO ES cells expressing either biotin-tagged MBD2a or MBD3a and identified known NuRD complex members using label-free mass spectrometry (Supplementary Fig. 8b-c). We then calculated the intensity-based absolute quantification (iBAQ) values of the most predominant and statistically significant MBD-interacting proteins in both cell lines, which can be used to estimate the relative abundance. While we observe very similar complex composition between MBD2a-NuRD and MBD3a-NuRD, peptides shared between SALL1-4 proteins show a preferred interaction with the MBD2a-NuRD complex.
2023-06-30 | PXD042407 | Pride
Project description:Mouse embryonic stem cells mutant for Mbd3, Sall4 and/or the related Sall1 pluripotency-associated factors were cultured in self-renewing and neural differentiation conditions and profiled by RNA-seq.
2016-08-09 | E-MTAB-4566 | biostudies-arrayexpress
Project description:Cell fate decision involves rewiring of the genome, but remains poorly understood at the chromatin level. We report a system to reprogramming somatic cells to pluripotency by four factor combination (Sall4, Esrrb, Jdp2, Glis1). Mechanism study demonstrate that the Sall4-NuRD axis plays a critical role in the early phase of reprogramming. These results identify a previously unrecognized role of NuRD in reprogramming, may help establish early chromatin closing as a pre-requisite step in cell fate control.
2022-10-12 | GSE199613 | GEO
Project description:Cell fate decision involves rewiring of the genome, but remains poorly understood at the chromatin level. We report a system to reprogramming somatic cells to pluripotency by four factor combination (Sall4, Esrrb, Jdp2, Glis1). Mechanism study demonstrate that the Sall4-NuRD axis plays a critical role in the early phase of reprogramming. These results identify a previously unrecognized role of NuRD in reprogramming, may help establish early chromatin closing as a pre-requisite step in cell fate control.
2022-10-12 | GSE199612 | GEO
Project description:Cell fate decision involves rewiring of the genome, but remains poorly understood at the chromatin level. We report a system to reprogramming somatic cells to pluripotency by four factor combination (Sall4, Esrrb, Jdp2, Glis1). Mechanism study demonstrate that the Sall4-NuRD axis plays a critical role in the early phase of reprogramming. These results identify a previously unrecognized role of NuRD in reprogramming, may help establish early chromatin closing as a pre-requisite step in cell fate control.
2022-10-12 | GSE199609 | GEO
Project description:SALL4 is a nuclear factor central to the maintenance of stem cell pluripotency and is a key component in HCC, a malignancy with no effective treatment. In cancer cells, SALL4 associates with NuRD to silence tumor suppressor genes such as PTEN. Here, we design a potent therapeutic SALL4 peptide (FFW) capable of antagonizing the SALL4-NURD interaction using systematic truncation and amino acid substitution studies. To understand the pathways affected by the peptide treatment, we performed RNA sequencing on cells treated with different peptides. Furthermore, to identify SALL4 DNA binding targets, we have performed CRUD-ChIP sequencing with SALL4 and H2K27Ac antibodies on HCC cell line SNU398.
2018-07-05 | GSE112729 | GEO
Project description:RNA-seq was performed for transcriptional analysis of wild-type mouse embryonic stem (ES) cells and an Mbd3 knockout line. Mbd3 is a core component of the Nucleosome Remodeling and Deacetylation (NuRD) complex, which modulates transcriptional heterogeneity and pluripotency gene expression in ES cells.
2012-05-04 | E-MTAB-997 | biostudies-arrayexpress
Project description:Maintenance of chromatin structure is essential to eukaryotic life; dysregulation is known to be causal for aberrant development and disease. The Mi-2/nucleosome remodeling and histone deacetylase (NuRD) complex is a multiprotein machine proposed to regulate chromatin structure by nucleosome remodeling and histone deacetylation activities. We identified the localization of MBD3, a component of Mi-2/NuRD complex, in two breast cancer cell lines (MCF7 and MDA-MB-231) using ChIP-Seq. MBD3 showed cell-type specific localization with overlap across cell lines being less than 50%. MBD3 localized across gene bodies, peaking around the transcription start site (TSS). Contrary to existing models, MBD3 preferentially associated with CpG rich promoters marked by H3K4me3. These data suggest that MBD3, and by extension the Mi-2/NuRD complex, may have roles in fine tuning expression for active genes. These data represent an important first step in defining regulatory mechanisms by which Mi-2/NuRD complex controls chromatin structure and gene expression. Identification of MBD3 localization in human breast cancer cell lines
2013-10-31 | E-GEOD-44737 | biostudies-arrayexpress