The role of Rif1 in ES cells
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE55129 | GEO | 2014/02/19
SECONDARY ACCESSION(S): PRJNA238588
REPOSITORIES: GEO
Similar Datasets
Project description:Purpose:The goals of this study are to understand the mechanisms underlying reduced self-renewal and loss of pluripotency by depletion of Rif1. Methods: We performed global gene expression analysis of Rif1 knockdown ES cell lines using Affymetrix 430 2.0 arrays, compared to shRNA controls. J1 ES cells were transfected with Control shRNA and Rif1 shRNA using lipofectamine 2000. Forty-eight hours after transfection, cells were collected for global gene expression analysis using Affymetrix mouse genome 430 2.0 array. Stable F1 Rif1 knockdown ES cells at passage 16 were used for long-term gene expression chip microarray using Affymetrix mouse genome 430 2.0 array.
2014-02-19 | E-GEOD-55129 | biostudies-arrayexpress
Project description:Rif1 depletion in mouse ES cells increases the populations derepressing 2-cell zygote-specific genes including Zscan4. We investigated the chromatin structural change in the Zscan4 gene loci, and found that this region was deprived of major histone modifications except for moderately coded by H3 lysine9 trimethylation. Rif1 depletion caused no significant alteration in DNA methylation and histone modifications including common active marks, but only a notable increase in H3K27Ac active mark in gene bodies and neighboring regions, indicating that atypical broad enhancer-like chromatin with semi-silent property has been emerged in Zscan4 gene loci.<BR>In this study, we used microarrays to present the global changes in gene expression caused by transient depletion of Rif1.
2020-09-19 | GSE158220 | GEO
Project description:Gene expression of Rif1-depleted ES cells
| PRJNA664379 | ENA
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:Compare the gene expression profiles of ESCs stably expressing control and KIAA1718 short hairpin RNA, using Affymetrix microarray. Mouse ES cells R1 were transformed with the respective lenti-virus expressing Luc shRNA or KIAA1718 shRNA1. The transformed ES cells were sorted for GFP. Total RNAs were extracted from cells using Trizol reagent (Invitrogen, Carlsbad, CA). For microarray experiments, RNA was processed and hybridized to Mouse Genome 430 2.0 arrays (Affymetrix) according to the manifacture’s instruction.
2009-11-03 | E-GEOD-18771 | biostudies-arrayexpress
Project description:Affymetrix 430 2.0 mouse arrays were used for expression analyses in undifferentiated and differentiated PGK12.1 ES cells. We found that the X:autosome expression ratios calculated from the mean expression values of X-linked and autosomal genes from microarrays was ~1.4 in undifferentiated female ES cells and then decreased to 1.2 in PGK12.1 cells after 15-day embryoid body differentiation. Thus, a substantial level of X upregulation is already evident in these ES cells prior to differentiation. Our findings based on Affymetrix expression arrays are consistent with microarray analysis from other labs and our RNA-seq analysis of mouse female PGK12.1 ES cells.
2013-02-15 | GSE44251 | GEO
Project description:The bHLH transcription factor Tfe3 is a powerful regulator of pluripotency and we report a genome-wide analysis of Tfe3 occupancy in mouse ES cells. Nuclear localization of Tfe3 is inhibited by a protein complex containing the tumor-suppressor Folliculin (Flcn) and we also determine Tfe3 binding sites in ES cells expressing an shRNA targeting Flcn. Specificity is controlled for by using unspecific IgGs and ES cells expressing an shRNA targeting Tfe3.
2013-04-10 | GSE39815 | GEO
Project description:Orphan nuclear receptor Esrrb is vital in maintaining ES cells and like Oct4, Sox2 and Nanog is essential for self-renewal and pluripotency. Esrrb functions in somatic cells via LBD/AF-2-dependent coactivator recruitment to target genes. Here we show that in ES cells coactivator recruitment is similarly required and identify Ncoa3 as the Esrrb coactivator needed for activation of its target genes. Ncoa3 is essential for self-renewal and the induction of pluripotency in reprogramming, and genome-wide analysis of Ncoa3 binding reveals extensive overlap with Esrrb and pluripotency factors along with marks of active genes. Mechanistically, we show Ncoa3 is specifically required to bridge RNApol2 to Esrrb. We thus identify a new member of the ES pluripotency network and describe Esrrb and Ncoa3 as key factors linking core pluripotency factors to the general transcription machinery. Three biological replicates each for control scrambled shRNA and Ncoa3 shRNA transfected E14 mouse ESCs. The global gene expression profiles of Ncoa3 knockdown cells were compared to control scrambled shRNA knockdown cells 4 days post-transfection.
2012-10-02 | E-GEOD-40192 | biostudies-arrayexpress
Project description:In order to investigate the cooperative roles of Pontin and Oct4 for self-renewal and pluripotency in mouse ES cells, we performed mRNA-sequencing analysis from mRNAs isolated from Pontin- and Oct4-depleted ES cells. This analysis provides insight into molecular mechanisms for maintaining ES cell identity. mRNA expression profiles of Pontinf/f; CreER ES cells at 0, 3, or 4 days post-treatment with OHT (wild type and Pontin-depleted ES cells) and ZHBTc4 ES cells at 2 days post-treatment with tetracycline (Oct4-depleted ESE cells) were examined by Illumina Hiseq2000.
2015-10-16 | E-MTAB-1953 | biostudies-arrayexpress
Project description:Orphan nuclear receptor Esrrb is vital in maintaining ES cells and like Oct4, Sox2 and Nanog is essential for self-renewal and pluripotency. Esrrb functions in somatic cells via LBD/AF-2-dependent coactivator recruitment to target genes. Here we show that in ES cells coactivator recruitment is similarly required and identify Ncoa3 as the Esrrb coactivator needed for activation of its target genes. Ncoa3 is essential for self-renewal and the induction of pluripotency in reprogramming, and genome-wide analysis of Ncoa3 binding reveals extensive overlap with Esrrb and pluripotency factors along with marks of active genes. Mechanistically, we show Ncoa3 is specifically required to bridge RNApol2 to Esrrb. We thus identify a new member of the ES pluripotency network and describe Esrrb and Ncoa3 as key factors linking core pluripotency factors to the general transcription machinery.
2012-10-02 | GSE37262 | GEO