Gain of chromatin loops marks the exit from naïve pluripotency – in-situ Hi-C data
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PROVIDER: PRJEB25516 | ENA |
REPOSITORIES: ENA
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Project description:Gain of chromatin loops marks the exit from naive pluripotency - ChIP seq for CTCF and Rad21
| PRJEB20728 | ENA
Project description:In-situ Hi-C data for mouse embryonic stem cells (ES cells, grown in the presence of FBS and LIF) and for NS cells.
2018-11-08 | E-MTAB-6591 | biostudies-arrayexpress
Project description:The genome of pluripotent stem cells adopts a unique three-dimensional architecture featuring weakly condensed heterochromatin and large nucleosome-free regions. Yet, it is unknown whether structural loops and contact domains display characteristics that distinguish embryonic stem cells (ESCs) from differentiated cell types. We used genome-wide chromosome conformation capture and super-resolution imaging to determine nuclear organization in mouse ESC and neural stem cell (NSC) derivatives. We found that loss of pluripotency is accompanied by widespread gain of structural loops. This general architectural change correlates with enhanced binding of CTCF and cohesins and more pronounced insulation of contacts across chromatin boundaries in lineage-committed cells. Reprogramming NSCs to pluripotency restores the unique features of ESC domain topology. Domains defined by the anchors of loops established upon differentiation are enriched for developmental genes. Chromatin loop formation is a pervasive structural alteration to the genome that accompanies exit from pluripotency and delineates the spatial segregation of developmentally regulated genes.
| S-EPMC6327227 | biostudies-literature
Project description:ChIP-seq to map the binding sites for CTCF and cohesin subunit Rad21 in the naive mES cells (46C cell line grown in the 2i/LIF condition) and in the neural stem cells (derived from the 46C ES cells using the mono-layer differentiation protocol, grown in the N2B27 medium these cells are Nestin+). The naive mES cells were grown in two different media (fetal bovine serum, FBS and 2i/LIF culture - naive pluripotency conditions) as detailed in the growth protocols.
2018-11-08 | E-MTAB-5732 | biostudies-arrayexpress
Project description:The formation of R-loops is a natural consequence of the transcription process, caused by invasion of the DNA duplex by nascent transcripts. These structures have been considered rare transcriptional by-products with potential harmful effects on genome integrity, due to the fragility of the displaced DNA coding strand. However R-loops may also possess beneficial effects as their widespread formation has been detected over CpG island promoters in human genes. Furthermore we have previously shown that R-loops are particularly enriched over G-rich terminator elements. These facilitate RNA polymerase II (Pol II) pausing prior to efficient termination. Here we reveal an unanticipated link between R-loops and RNA interference (RNAi)-dependent H3K9me2 formation over pause site termination regions of mammalian protein coding genes. We show that R-loops induce antisense transcription over these pause elements which in turn lead to the generation of double-strand RNA (dsRNA) and recruitment of Dicer, Ago1, Ago2, and G9a histone lysine methyltransferase (HKMT). Consequently an H3K9me2 repressive mark is formed and Heterochromatin Protein 1γ (HP1γ) is recruited, that reinforces Pol II pausing prior to efficient transcriptional termination. We predict that R-loops promote a chromatin architecture that defines the termination region for a substantial subset of mammalian genes. PolIIS2ph ChIP-seq and input in untreated condition and treated with BIX and RNaseH1 overexpression in HeLa cells. The 4 samples have been multiplexed, pooled and sequenced on 3 lanes of Illumina HiSeq2000.
2014-09-29 | E-GEOD-59878 | biostudies-arrayexpress
Project description:R-loops are transcription by-products that may constitute a threat to genome integrity. In addition to specific enzymes to remove them, eukaryotes rely on a number of mRNP biogenesis factors such as the THO complex, to prevent co-transcriptional R-loop formation. We show in Saccharomyces cerevisiae that R-loops are tightly and specifically linked with histone H3-Ser10 phosphorylation (H3S10P), a mark of chromatin condensation. Importantly, ChIP-chip analyses reveal a clear H3S10P accumulation at the pericentromeric chromatin during the G1-phase of the cell cycle only in R loop-accumulating yeast strains but not in those non-accumulating R-loops, and a significantly higher accumulation during S-phase. Such a difference can also be detected in a number of genes along the genome. ChIP-chip studies were perfomed with antibodies against Histone H3 and the phosphorylated Histone H3 at Serine10 in the yeast S. cerevisiae.
2013-11-13 | E-GEOD-46627 | biostudies-arrayexpress
Project description:The formation of R-loops is a natural consequence of the transcription process, caused by invasion of the DNA duplex by nascent transcripts. These structures have been considered rare transcriptional by-products with potential harmful effects on genome integrity, due to the fragility of the displaced DNA coding strand. However R-loops may also possess beneficial effects as their widespread formation has been detected over CpG island promoters in human genes. Furthermore we have previously shown that R-loops are particularly enriched over G-rich terminator elements. These facilitate RNA polymerase II (Pol II) pausing prior to efficient termination. Here we reveal an unanticipated link between R-loops and RNA interference (RNAi)-dependent H3K9me2 formation over pause site termination regions of mammalian protein coding genes. We show that R-loops induce antisense transcription over these pause elements which in turn lead to the generation of double-strand RNA (dsRNA) and recruitment of Dicer, Ago1, Ago2, and G9a histone lysine methyltransferase (HKMT). Consequently an H3K9me2 repressive mark is formed and Heterochromatin Protein 1γ (HP1γ) is recruited, that reinforces Pol II pausing prior to efficient transcriptional termination. We predict that R-loops promote a chromatin architecture that defines the termination region for a substantial subset of mammalian genes.
2014-09-29 | GSE59878 | GEO
Project description:R-loops are transcription by-products that may constitute a threat to genome integrity. In addition to specific enzymes to remove them, eukaryotes rely on a number of mRNP biogenesis factors such as the THO complex, to prevent co-transcriptional R-loop formation. We show in Saccharomyces cerevisiae that R-loops are tightly and specifically linked with histone H3-Ser10 phosphorylation (H3S10P), a mark of chromatin condensation. Importantly, ChIP-chip analyses reveal a clear H3S10P accumulation at the pericentromeric chromatin during the G1-phase of the cell cycle only in R loop-accumulating yeast strains but not in those non-accumulating R-loops, and a significantly higher accumulation during S-phase. Such a difference can also be detected in a number of genes along the genome.
2013-11-13 | GSE46627 | GEO
Project description:Cohesin catalyses the folding of the genome into loops that are anchored by CTCF. The molecular mechanism of how cohesin and CTCF structure the 3D genome has remained unclear. Here we show that a segment within the CTCF N terminus interacts with the SA2-SCC1 subunits of cohesin. A 2.6 Å crystal structure of SA2-SCC1 in complex with CTCF reveals the molecular basis of the interaction. We demonstrate that this interaction is specifically required for CTCF-anchored loops and contributes to the positioning of cohesin at CTCF-binding sites. A similar motif is present in a number of established and novel cohesin ligands, including the cohesin release factor WAPL. Our data suggest that CTCF enables chromatin loop formation by protecting cohesin against loop release. These results provide fundamental insights into the molecular mechanism that enables dynamic regulation of chromatin folding by cohesin and CTCF.
2020-01-07 | GSE126636 | GEO
Project description:We sought to examine whether the non-canonical SMC protein Smchd1 plays a role in chromosome conformation. We used in situ Hi-C to analyse chromosome conformation changes upon deletion of the epigenetic regulator Smchd1 in female neural stem cells. In parallel, we analysed nucleosome accessibility using ATAC-seq, gene expression using RNA-seq, chromatin marks H3K27me3 and H3K27ac and Ctcf binding using ChIP-seq. We additionally analysed Smchd1 binding genome-wide using ChIP-seq. Together, we find that deletion of Smchd1 alters chromosome conformation at Smchd1 target genes including the inactive X chromosome, Hox genes and imprinted loc. Smchd1 deletion results in gain in Ctcf binding and activation of enhancers. We propose Smchd1 functions by limiting Ctcf-mediated chromosome looping.
2018-06-30 | GSE111720 | GEO