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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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RNA-seq of wild-type, Mbd3 and Sall4/1 mutant mouse embryonic stem cells

ABSTRACT: 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.

INSTRUMENT(S): Illumina HiSeq 2500

ORGANISM(S): Mus musculus

SUBMITTER: Paul Bertone

PROVIDER: E-MTAB-4566 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Sall4 controls differentiation of pluripotent cells independently of the Nucleosome Remodelling and Deacetylation (NuRD) complex.

Miller Anzy A Ralser Meryem M Kloet Susan L SL Loos Remco R Loos Remco R Nishinakamura Ryuichi R Bertone Paul P Vermeulen Michiel M Hendrich Brian B

Development (Cambridge, England) 20160728 17

Sall4 is an essential transcription factor for early mammalian development and is frequently overexpressed in cancer. Although it is reported to play an important role in embryonic stem cell (ESC) self-renewal, whether it is an essential pluripotency factor has been disputed. Here, we show that Sall4 is dispensable for mouse ESC pluripotency. Sall4 is an enhancer-binding protein that prevents precocious activation of the neural gene expression programme in ESCs but is not required for maintenanc ...[more]

PMID: 27471257

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ChIP-seq of NuRD components and pluripotency factors in wild-type, Mbd3 and Sall4/1 mutant embryonic stem cells

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

Stoichiometry of MBD2 vs. MBD3-NuRD

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

Differential roles of Sall4 isoforms in ES cell pluripotency

Project description:This SuperSeries is composed of the following subset Series: GSE21054: Differential roles of Sall4 isoforms in ES cell pluripotency: expression GSE21055: Differential Role of Sall4 isoforms in ES cell pluripotency: ChIP-chip Refer to individual Series

2010-09-13 | E-GEOD-21056 | biostudies-arrayexpress

A key role for Mbd3 in 5-hydroxymethylcytosine-dependent gene regulation in embryonic stem cells

Project description:Numerous chromatin regulators are required for embryonic stem (ES) cell self-renewal and pluripotency, but few have been studied in detail. Here, we examine the roles of several chromatin regulators whose loss affects the pluripotent state of ES cells. We find that Mbd3 and Brg1 antagonistically regulate a common set of genes by regulating promoter-proximal nucleosome occupancy and recruitment of RNA polymerase II. Furthermore, both Mbd3 and Brg1 play key roles in the biology of 5-hydroxymethylcytosine (5hmC): Mbd3 colocalizes with both Tet1 and 5hmC in vivo, its localization is Tet1-dependent, and binding of Mbd3/NURD to DNA in vitro is inhibited by methylcytosine, but not hydroxymethylcytosine. Finally, both Mbd3 and Brg1 are themselves required for normal levels of 5hmC in vivo. Together, our results identify an effector for 5hmC, and reveal that control of gene expression by antagonistic chromatin regulators is a surprisingly common regulatory strategy in ES cells. Genomic binding profiles of Mbd3 in normal ES cells, along with ES cells depleted of additional chromatin regulators, Brg1 and Tet1 were performed by ChIP-seq. In addition, we performed mapping of RNA Polymerase II in control (EGFP), Mbd3 and Brg1 knockdown ES cells by ChIP-seq.

2011-12-01 | E-GEOD-31690 | biostudies-arrayexpress

Expression profile of Sall4-null ES cells and Sall4 heterozygous ES cells

Project description:Sall4 is a mouse homolog of a causative gene of the autosomal dominant disorder known as Okihiro syndrome. We previously showed that Sall4 absence leads to lethality during peri-implantation and that Sall4-null embryonic stem (ES) cells proliferate poorly with intact pluripotency when cultured on feeder cells. However, a subsequent report indicated that shRNA-mediated Sall4 inhibition in ES cells led to a severe reduction in Oct3/4 and a secondary increase in Cdx2, which resulted in complete differentiation into the trophectoderm when cultured in the feeder-free condition. So we profiled gene expression changes when Sall4 is deleted in ES cells in the presence or absence of feeder cells. key word: embryonic stem (ES) cell, Sall4, feeder ES cells were cultured with or without mouse embryonic fibroblast (MEF) feeder cells in LIF-supplemented medium as described. To maintain the expression of Oct3/4, all ES cells were cultured in the presence of Blasticidin. Four samples were analyzed. GSM356329, GSM356330 : cultured in the absence of feeders GSM356331, GSM356332 : cultured on the feeders

2009-04-01 | E-GEOD-14219 | biostudies-arrayexpress

RNA-seq of wild-type, Mbd3 and Sall4/1 mutant mouse embryonic stem cells

Project description:RNA-seq of wild-type, Mbd3 and Sall4/1 mutant mouse embryonic stem cells

| PRJEB13071 | ENA

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

Transcriptional profiling of Mbd3 knockout and wild-type embryonic stem cells

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

Expression profile of Sall4-null ES cells and Sall4 heterozygous ES cells

2009-04-01 | GSE14219 | GEO

ChIP-seq analysis of MBD3 in human breast cancer cells

Project description:Chromatin immunoprecipitation followed by massively parallel sequencing (ChIP-seq) is a powerful approach to identify the genome-wide localization of protein of interest. However, to perform ChIP-seq experiments for large protein complex, such as Mi-2/NuRD complex, is still challenging. Here, we present high-quality MBD3 ChIP-seq data in human breast cancer cells, MDA-MB-231. MBD3 ChIP-seq experiment was perform using human breast cancer cells, MDA-MB-231. Two bilogical replicates were prepared.

2015-12-21 | E-GEOD-76116 | biostudies-arrayexpress

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