Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression of Rif1-depleted ES cells

ABSTRACT: 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.
In this study, we used microarrays to present the global changes in gene expression caused by transient depletion of Rif1.

ORGANISM(S): Mus musculus

PROVIDER: GSE158220 | GEO | 2020/09/19

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Genome-wide maps of H3K9me3 in control ESCs and Rif1 knockdown ESC.

Project description:We found that Rif1 depletion leads to reduced H3K9me3 levels at 1/3 of the H3K9me3-enriched genomic regions (H3K9me3 peaks), and that reduced H3K9me3 de-represses Zscan4 and other genes that are specific to the 2-Cell stage embryo. Examination of H3K9me3 histone modifications in 2 cell types.

2014-02-13 | E-GEOD-54947 | biostudies-arrayexpress

Genome-wide maps of H3K9me3 in control ESCs and Rif1 knockdown ESC.

2014-02-13 | GSE54947 | GEO

The role of Rif1 in ES cells

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

The role of Rif1 in ES cells

2014-02-19 | GSE55129 | GEO

Genome-wide distribution of histones modifications in mouse ESC Rif1+/+ and Rif1-/-

Project description:Genome-wide distribution of histones modifications in mouse ESC Rif1+/+ and Rif1-/-

| PRJEB9864 | ENA

Rif1 functions in complex with PRC1.6 to regulate mouse embryonic stem cells fate potential [ChIP-seq]

Project description:To investigate if Rif1 depletion compromised the accurate genomic targeting of the PRC1.6 complex, we performed ChIP-seq analyses of Rif1, Pcgf6, RNF2, and the H2AK119ub in the control and Rif1-depleted mESCs.

2022-06-10 | GSE203304 | GEO

Rif1 regulates the replication timing domains on the human genome

Project description:DNA replication is spatially and temporally regulated during S-phase. DNA replication timing is established in early G1-phase at a point referred to as TDP (timing decision point). We show that Rif1 (Rap1-interacting-factor1), originally identified as a telomere binding factor in yeast, is a critical determinant of the replication timing program in human cells. Depletion of Rif1 results in specific loss of mid-S replication foci profiles, stimulation of initiation events in early S-phase and changes in long-range replication timing domain structures. Overall replication timing is shifted toward mid-S in both directions, suggesting that replication timing regulation is abrogated in the absence of Rif1. Rif1 tightly binds to nuclear insoluble structures at late-M to early-G1 and regulates the chromatin-loop sizes. Furthermore, Rif1 colocalizes specifically with the mid-S replication foci. Thus, Rif1 establishes the mid-S replication domains that are restrained from being activated at early S-phase. Our results indicate that Rif1 plays crucial roles in determining the replication timing domain structures through regulating higher-order chromatin architecture. HeLa cells (ATCC), with a total of 4 individual replicates

2012-05-14 | E-GEOD-37971 | biostudies-arrayexpress

Rif1 inhibits replication fork progression and controls copy number in Drosophila.

Project description:Control of DNA copy number is essential to maintain genome stability and ensure proper cell and tissue function. In Drosophila, the SNF2-domain-containing SUUR protein inhibits replication fork progression within specific regions of the genome to promote DNA underreplication. While dissecting the function of SUUR’s SNF2 domain, we identified a physical interaction between SUUR and Rif1. Rif1 has many roles in DNA metabolism and regulates the replication timing program. We demonstrate that repression of DNA replication is dependent on Rif1. Rif1 localizes to active replication forks in an SUUR-dependent manner and directly regulates replication fork progression. Importantly, SUUR associates with replication forks in the absence of Rif1, indicating that Rif1 acts downstream of SUUR to inhibit fork progression. Our findings uncover an unrecognized function of the Rif1 protein as a direct regulator of replication fork progression suggesting developmental regulation of Rif1 activity.

2018-10-15 | GSE114370 | GEO

Rif1 regulates the replication timing domains on the human genome

2012-05-15 | GSE37971 | GEO

Rif1 and Hmgn3 Regulate Conversion of Murine Trophoblast Stem Cells

Project description:The arising of trophectoderm (TE) is a hallmark event in preimplantation development during embryogenesis. However, little is known about the mechanisms underlying TE specification. Our findings demonstrate that depletion of Rif1 breaks down the barriers to conversion of trophoblast stem cells (TSCs). Rif1-null induced TSCs show typical TE properties, and differentiation potentials to terminal trophoblast lineages. Global transcriptome analysis reveals that Rif1-null activates 2-cell embryo (2C) related genes and induces a totipotent-like state, which is probably the main reason for the conversion of TSCs from Rif1-null embryonic stem cells (ESCs). Chimeric assays further confirm that Rif1-null ESCs can contribute to TE, further yielding TSCs in vitro. Over-expression of a downstream gene of Rif1, Hmgn3, can also activate 2C related genes and facilitate induction of TSCs. Here, we report two pioneer genes regulating conversion of TSCs and provide insights for investigating the mechanisms of TE specification.

2021-12-01 | GSE189683 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data