Ontology highlight
ABSTRACT:
PROVIDER: PRJNA268117 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1636750_1.fastq.gz | Fastqsanger.gz | |||
| SRR1636750_2.fastq.gz | Fastqsanger.gz | |||
| SRR1636760_1.fastq.gz | Fastqsanger.gz | |||
| SRR1636760_2.fastq.gz | Fastqsanger.gz | |||
| SRR1636770_1.fastq.gz | Fastqsanger.gz |
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Project description:Widespread rearrangement of 3D chromatin organization underlies Polycomb-mediated stress-induced silencing [ChIP]
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Project description:Widespread rearrangement of 3D chromatin organization underlies Polycomb-mediated stress-induced silencing [Hi-C]
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Project description:Interphase chromatin is organized into topologically associating domains (TADs). Within TADs, chromatin looping interactions are formed between DNA regulatory elements, but their functional importance for the establishment of the 3D genome organization and gene regulation during development is unclear. Using high-resolution Hi-C experiments, we analyze higher order 3D chromatin organization during Drosophila embryogenesis and identify active and repressive chromatin loops that are established with different kinetics and depend on distinct factors: Zelda-dependent active loops are formed before the midblastula transition between transcribed genes over long distances. Repressive loops within polycomb domains are formed after the midblastula transition between polycomb response elements by the action of GAGA factor and polycomb proteins. Perturbation of PRE function by CRISPR/Cas9 genome engineering affects polycomb domain formation and destabilizes polycomb-mediated silencing. Preventing loop formation without removal of polycomb components also decreases silencing efficiency, suggesting that chromatin architecture can play instructive roles in gene regulation during development.
2018-06-08 | GSE103625 | GEO
Project description:Spermatogenesis is a unidirectional differentiation process that generates haploid sperm, but how the gene expression program that directs this process is established is largely unknown. Here we determine the high-resolution 3D chromatin architecture of male germ cells during spermatogenesis and show that CTCF-mediated 3D chromatin predetermines the gene expression program required for spermatogenesis. In undifferentiated spermatogonia, CTCF-mediated chromatin interactions between meiosis-specific super-enhancers (SE) loci and target genes precede activation of meiosis-specific SEs on autosomes. These meiotic SE recruit the master transcription factor A-MYB in meiotic spermatocytes, which strengthens their 3D contacts and instructs a burst of meiotic gene expression. We also find that at the mitosis-to-meiosis transition, the germline-specific Polycomb protein SCML2 resolves chromatin loops that are specific to mitotic spermatogonia. Moreover, SCML2 and A-MYB establish the unique 3D chromatin organization of sex chromosomes during meiotic sex chromosome inactivation. We propose that CTCF-mediated 3D chromatin organization enforces epigenetic priming that directs unidirectional differentiation, thereby determining the cellular identity of the male germline.
2024-12-13 | GSE272432 | GEO
Project description:Polycomb Repressive Complexes 1 and 2 (PRC1, PRC2) are conserved epigenetic regulators that promote transcriptional silencing. PRC1 and PRC2 converge on shared targets, catalyzing repressive histone modifications. In addition, a subset of PRC1/PRC2 targets engage in long-range interactions whose functions in gene silencing are poorly understood. Using a CRISPR screen in mouse embryonic stem cells, we discovered that the cohesin regulator PDS5A links transcriptional silencing by Polycomb and 3D genome organization. PDS5A deletion impairs cohesin unloading and results in derepression of subset of endogenous PRC1/PRC2 target genes. Importantly, derepression is not associated with loss of repressive Polycomb chromatin modifications. Instead, loss of PDS5A leads to aberrant cohesin activity, ectopic insulation sites and specific reduction of ultra-long Polycomb loops. We infer that these loops are important for robust silencing at a subset of Polycomb target genes and that maintenance of cohesin-dependent genome architecture is critical for Polycomb regulation.
2023-11-10 | GSE194268 | GEO
Project description:Polycomb group (PcG) proteins dynamically define cellular identities through epigenetic repression of key developmental genes. PcG target gene repression can be stabilized through the interaction in the nucleus at PcG foci. Here, we report the results of a high-resolution microscopy genome-wide RNAi screen that identifies 129 genes that regulate the nuclear organization of Pc foci. Candidate genes include PcG components and chromatin factors, as well as many novel protein-modifying enzymes, including components of the SUMOylation pathway. In the absence of SUMO Pc foci coagulate into larger aggregates. Conversely, loss of function of the SUMO peptidase velo disperses Pc foci. Moreover, SUMO and velo colocalize with PcG proteins at PREs and Pc SUMOylation affects its chromatin targeting, suggesting that the dynamic regulation of Pc SUMOylation regulates PcG-mediated silencing by modulating the kinetics of Pc binding to chromatin as well as its ability to form Polycomb foci. ChIP-Seq mapping of Polycomb (PC), SUMO and Velo on Drosophila Melanogaster
2014-04-03 | E-GEOD-55303 | biostudies-arrayexpress
Project description:Polycomb (PcG) silencing is crucial for development, but how targets are specified remains incompletely understood. The cold-induced Polycomb Repressive Complex 2 (PRC2) silencing of Arabidopsis thaliana FLOWERING LOCUS C (FLC) provides an excellent system to elucidate PcG regulation. Association of the DNA binding protein VAL1 to the PcG nucleationregion at FLC is an important step. VAL1 interacts with APOPTOSIS AND SPLICING ASSOCIATED PROTEIN (ASAP) complex and PRC1. Here, we show that ASAP and PRC1 are necessary for co-transcriptional repression and chromatin regulation during FLC silencing. ASAP mutants affect FLC transcription in warm conditions, but the rate of FLC silencing in the cold is unaffected. PRC1-mediated H2Aub accumulates at FLC nucleation region during cold, but unlike the PRC2-delivered H3K27me3 does not spread across the locus. H2Aub thus marks the transition to epigenetic silencing, while H3K27me3 is necessary for long-term epigenetic memory. Overall, our work highlights the importance of VAL1 as an assembly platform co-ordinating the co-transcriptional repression and chromatin regulation necessary for the epigenetic silencing of FLC.
2022-08-15 | PXD036057 |
Project description:• Polycomb (PcG) regulation is crucial for development across eukaryotes, but how PcG targets are specified is still incompletely understood. The slow timescale of cold-induced Polycomb Repressive Complex 2 silencing during vernalization at Arabidopsis thaliana FLOWERING LOCUS C (FLC) provides an excellent system to elucidate the sequence of events. Association of the DNA binding protein VAL1 to an FLC intronic RY motif within the PcG nucleation region is an important step. VAL1 is associated in vivo with APOPTOSIS AND SPLICING ASSOCIATED PROTEIN (ASAP) complex and Polycomb Repressive Complex 1 (PRC1). Here, we show that ASAP and PRC1 functions are necessary for co-transcriptional repression and chromatin regulation during FLC silencing. ASAP mutants affect FLC transcription in warm conditions, but the rate of FLC silencing in the cold is unaffected. PRC1-mediated H2Aub accumulation increases at the nucleation region upon exposure to cold, but unlike the PRC2-delivered H3K27me3 does not spread across the locus. H2Aub is thus involved in the transition to epigenetic silencing at FLC facilitating H3K27me3 accumulation, which in turn is necessary for long-term epigenetic memory. Overall, our work highlights the importance of the DNA sequence-specific binding protein VAL1 as an assembly platform coordinating the co-transcriptional repression and chromatin regulation necessary for the epigenetic silencing of FLC.
2022-10-13 | PXD036548 | Pride
Project description:Characterizing the relationship between genome form and function requires methods both for zooming out, to globally survey the genomic architectural landscape, and for zooming in, to investigate regions of interest at high resolution. High throughput methods based on chromosome conformation capture (3C) have greatly advanced our understanding of the three-dimensional (3D) organization of genomes, but are limited in resolution by their reliance on restriction enzymes. Here we describe a method for comprehensively mapping global chromatin contacts that uses DNaseI for chromatin fragmentation, leading to greatly improved efficiency and resolution. Coupling this method with DNA capture technology provides a high-throughput approach for targeted mapping of fine-scale chromatin architecture. We applied targeted DNase Hi-C to characterize the 3D organization of 1,030 lincRNA promoters in two human cell lines, and identified thousands of high-confidence lincRNA promoter-associated chromatin contacts at 1 kilobase pair (kbp) resolution. Detailed analysis of these contacts reveals that expression of lincRNAs is tightly controlled by complex mechanisms involving both super-enhancers and the polycomb repressive complex. Our results provide the first glimpse of the cell-type-specific 3D organization of lincRNA genes. DNase Hi-C assay (x1 replicate) in H1 and K562 cells, respectively. Targeted DNase Hi-C assays of the 220kb promoter-enhancer library (x1 replicate) and the 5Mb lincRNA promoter library (x2 replicate), in H1 and K562 cells, respectively.
2014-11-01 | E-GEOD-56869 | biostudies-arrayexpress
Project description:Chromatin is organized into a 3D interwoven tapestry of multi-layer architectural features important for controlling gene expression. How distinct layers influence each other and quickly they quickly they respond to cellular environment is unclear. Using Hi-C in Drosophila melanogaster, we measure how 3D chromatin organization responds to cellular hyperosmotic stress. In combination with the hd-pairing method, we demonstrate that chromosome unpairing represents a fast an reversible response to hyperosmotic stress. We identify a novel function of the Z4 protein as an anti-pairer, which we demonstrate is necessary for changes to chromatin organization during hyperosmotic stress. Finally, we demonstrate how changes to pairing impacts the other interwoven layers of 3D chromatin organization.
2024-03-19 | GSE213552 | GEO