Genome-wide maps of H3K9me3 in control ESCs and Rif1 knockdown ESC.
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE54947 | GEO | 2014/02/13
SECONDARY ACCESSION(S): PRJNA238127
REPOSITORIES: GEO
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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
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.
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Project description:Genome-wide distribution of histones modifications in mouse ESC Rif1+/+ and Rif1-/-
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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:DNA is replicated in a defined temporal order termed the replication timing (RT) program, which is correlated with genome compartmentalization with early replicating chromatin located mainly in the A compartment and late replicating chromatin in the B compartment (Dixon et al 2012, Moindrot et al 2012, Ryba et al 2010, Yaffe et al 2010). Similarly, active histone modifications and transcriptional permissiveness are associated with early replication while a repressive chromatin state is associated with late replication (Hiratani et al 2009, Riveria-Mulia et al 2015, Lubelsky et al 2014). However, the mechanistic interplay between RT, chromatin state, and genome compartmentalization is largely unknown. Here we report RT is upstream of epigenome formation and compartmentalisation in human embryonic stem cells (hESCs) and the cancer cell line HCT116. Knockout (KO) of the conserved RT control factor RIF1, rather than causing discrete RT switches, leads to dramatically increased cell to cell heterogeneity of RT genome wide, despite RIF1’s enrichment in late replicating chromatin. RIF1 KO hESCs have a nearly random RT program, unlike any other cell type to date, yet cells self-renew without signs of differentiation. Those regions that do retain RT consist of large H3K9me3 domains, which are prevalent in HCT116 but rare in hESCs, revealing two independent mechanisms of RT regulation that are used to different extents in different cell types. RIF1 KO cells also showed genome wide downregulation of H3K27ac peaks and enrichment of H3K9me3 at large domains that remained late replicating, while H3K27me3 and H3K4me3 were also re-distributed genome wide but in a cell type specific manner. Histone modification changes correlated with gene expression changes and global reorganisation of genome compartments. Some RT/compartment shifts were associated with specific TAD boundary shifts, but overall we observed a genome wide strengthening of TAD structures. Our findings support a model in which RT controlled by RIF1 plays a key role in establishing epigenetic state and genome architecture in human cells.
2021-04-26 | GSE160563 | GEO
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.
2014-02-19 | GSE55129 | GEO
Project description:We report the application of single-molecule-based sequencing technology for high-throughput profiling of histone modifications in mammalian cells and characterized genome-wide SetDB1 binding and H3K9 trimethylation (H3K9me3) profiles in mouse ES cells and uncovered two distinct classes of SetDB1 binding sites, termed solo and ensemble peaks. The solo peaks were devoid of H3K9me3 and enriched near developmental regulators while the ensemble peaks were associated with H3K9me3. A subset of the SetDB1 solo peaks, particularly those near neural development related genes, was found to be associated with Polycomb Repressive Complex 2 (PRC2) as well as PRC2-interacting proteins Jarid2 and Mtf2. Genetic deletion of Setdb1 dramatically reduced Ezh2 binding as well as histone 3 lysine 27 (H3K27) trimethylation level at SetDB1 solo peaks and facilitated neural differentiation. Furthermore, we found that H3K27me3 inhibits SetDB1 methyltransferase activity in vitro. The currently identified reciprocal action between SetDB1 and PRC2 reveals a novel mechanism underlying ES cell pluripotency and differentiation regulation. Examination of 2 different histone modifications in 2 cell status.
2015-06-25 | E-GEOD-62666 | biostudies-arrayexpress
Project description:Transposable elements, including endogenous retroviruses (ERVs), constitute a large fraction of the mammalian genome. They are transcriptionally silenced during early development to protect genome integrity and aberrant transcription. However, the mechanisms that control their repression are not fully understood. To systematically study ERV repression, we carried out an RNAi screen in mouse embryonic stem cells (ESCs) and identified a list of novel regulators. Among them, Rif1 displays the strongest effect. Rif1 depletion by RNAi or gene deletion led to increased transcription and increased chromatin accessibility at ERV regions and their neighboring genes. This transcriptional de-repression becomes more severe when DNA methylation is lost. On the mechanistic level, Rif1 directly occupies ERVs and is required for repressive histone mark H3K9me3 and H3K27me3 assembly and DNA methylation. It interacts with histone methyltransferases and facilitates their recruitment to ERV regions. Importantly, Rif1 represses ERVs in human ESCs as well, and the evolutionally-conserved HEAT-like domain is essential for its function. Finally, Rif1 acts as a barrier during somatic cell reprogramming, and its depletion significantly enhances reprogramming efficiency. Together, our study uncovered many previously uncharacterized repressors of ERVs, and defined an essential role of Rif1 in the epigenetic defense against ERV activation.
2017-09-19 | GSE98255 | GEO
Project description:Transposable elements, including endogenous retroviruses (ERVs), constitute a large fraction of the mammalian genome. They are transcriptionally silenced during early development to protect genome integrity and aberrant transcription. However, the mechanisms that control their repression are not fully understood. To systematically study ERV repression, we carried out an RNAi screen in mouse embryonic stem cells (ESCs) and identified a list of novel regulators. Among them, Rif1 displays the strongest effect. Rif1 depletion by RNAi or gene deletion led to increased transcription and increased chromatin accessibility at ERV regions and their neighboring genes. This transcriptional de-repression becomes more severe when DNA methylation is lost. On the mechanistic level, Rif1 directly occupies ERVs and is required for repressive histone mark H3K9me3 and H3K27me3 assembly and DNA methylation. It interacts with histone methyltransferases and facilitates their recruitment to ERV regions. Importantly, Rif1 represses ERVs in human ESCs as well, and the evolutionally-conserved HEAT-like domain is essential for its function. Finally, Rif1 acts as a barrier during somatic cell reprogramming, and its depletion significantly enhances reprogramming efficiency. Together, our study uncovered many previously uncharacterized repressors of ERVs, and defined an essential role of Rif1 in the epigenetic defense against ERV activation.
2017-09-19 | GSE98253 | GEO
Project description:Transposable elements, including endogenous retroviruses (ERVs), constitute a large fraction of the mammalian genome. They are transcriptionally silenced during early development to protect genome integrity and aberrant transcription. However, the mechanisms that control their repression are not fully understood. To systematically study ERV repression, we carried out an RNAi screen in mouse embryonic stem cells (ESCs) and identified a list of novel regulators. Among them, Rif1 displays the strongest effect. Rif1 depletion by RNAi or gene deletion led to increased transcription and increased chromatin accessibility at ERV regions and their neighboring genes. This transcriptional de-repression becomes more severe when DNA methylation is lost. On the mechanistic level, Rif1 directly occupies ERVs and is required for repressive histone mark H3K9me3 and H3K27me3 assembly and DNA methylation. It interacts with histone methyltransferases and facilitates their recruitment to ERV regions. Importantly, Rif1 represses ERVs in human ESCs as well, and the evolutionally-conserved HEAT-like domain is essential for its function. Finally, Rif1 acts as a barrier during somatic cell reprogramming, and its depletion significantly enhances reprogramming efficiency. Together, our study uncovered many previously uncharacterized repressors of ERVs, and defined an essential role of Rif1 in the epigenetic defense against ERV activation.
2017-09-19 | GSE98254 | GEO