Ontology highlight
ABSTRACT:
PROVIDER: PRJNA384993 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5489110.fastq.gz | Fastqsanger.gz | |||
| SRR5489111.fastq.gz | Fastqsanger.gz | |||
| SRR5489112.fastq.gz | Fastqsanger.gz | |||
| SRR5489113.fastq.gz | Fastqsanger.gz | |||
| SRR5489114.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
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Project description:Eukaryotic chromosomes are partitioned into topologically associating domains (TADs) that are demarcated by distinct insulator-binding proteins (IBPs) in Drosophila. Whether IBPs regulate specific long-range contacts and how this may impact gene expression remains unclear. Here we identify ‘indirect peaks’ of multiple IBPs, that represent their distant sites of interactions through long-range contacts. Indirect peaks depend on protein-protein interactions among multiple IBPs and their common co-factors, including CP190, as confirmed by high-resolution analyses of long-range contacts. Mutant IBPs unable to interact with CP190 impair long-range contacts as well as the expression of hundreds of distant genes that are specifically flanked by indirect peaks. Regulation of distant genes strongly correlates with RNAPII pausing, highlighting how this key transcriptional stage may trap insulator-based long-range interactions. Our data illustrate how indirect peaks may decipher gene regulatory networks through specific long-range interactions. Binding profiles of Beaf-32 in Drosophila S2 cells by ChIP-Seq (Illumina)
2014-02-01 | E-GEOD-52962 | biostudies-arrayexpress
Project description:Eukaryotic chromosomes are partitioned into topologically associating domains (TADs) that are demarcated by distinct insulator-binding proteins (IBPs) in Drosophila. Whether IBPs regulate specific long-range contacts and how this may impact gene expression remains unclear. Here we identify ‘indirect peaks’ of multiple IBPs, that represent their distant sites of interactions through long-range contacts. Indirect peaks depend on protein-protein interactions among multiple IBPs and their common co-factors, including CP190, as confirmed by high-resolution analyses of long-range contacts. Mutant IBPs unable to interact with CP190 impair long-range contacts as well as the expression of hundreds of distant genes that are specifically flanked by indirect peaks. Regulation of distant genes strongly correlates with RNAPII pausing, highlighting how this key transcriptional stage may trap insulator-based long-range interactions. Our data illustrate how indirect peaks may decipher gene regulatory networks through specific long-range interactions. Binding profiles of CP190 in stably transfected Drosophila S2 cell lines expressing in Wild-Type Beaf (Control) or Mutant Beaf by ChIP-Seq (Illumina)
2014-02-01 | E-GEOD-52886 | biostudies-arrayexpress
Project description:Chromatin insulators are DNA-protein complexes situated throughout the genome that contribute to higher order organization and demarcation into distinct transcriptional domains. Mounting evidence in different species implicates RNA and RNA-binding proteins as regulators of chromatin insulator activities. Here we identify the Drosophila hnRNP M homolog Rumpelstiltskin (Rump) as an antagonist of gypsy chromatin insulator enhancer-blocking and barrier activities. Despite ubiquitous expression of Rump, improvement of barrier activity is detected only in tissue outside of the central nervous system (CNS) when Rump levels are reduced. Furthermore, rump mutants restore insulator complex localization in an otherwise compromised genetic background only in non-CNS tissues. Rump associates physically with core gypsy insulator proteins, and ChIP-Seq analysis of Rump demonstrates extensive colocalization with a subset of gypsy insulator sites across the genome. The genome-wide binding profile and tissue-specificity of Rump contrast with that of Shep, a recently identified RNA-binding protein that antagonizes gypsy insulator activity exclusively in the CNS. Our findings indicate parallel roles for RNA-binding proteins in mediating tissue-specific regulation of chromatin insulator activity. ChIP-seq of Rump, Mod(mdg4)2.2, Shep, Su(Hw), and CP190 in Drosophila Kc167 cells
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Project description:Estrogen receptor M-NM-1 (ERM-NM-1) is key player in the progression of breast cancer. ERM-NM-1 binds to DNA and mediates long-range chromatin interactions throughout the genome, but the underlying mechanism in this process is unclear. Here, we show that AP-2 motifs are highly enriched in the ERM-NM-1 binding sites (ERBS) identified from the recent ChIA-PET of ERM-NM-1. More importantly, we demonstrate that AP-2M-NM-3 (also known as TFAP2C), a member of the AP-2 family which has been implicated in breast cancer oncogenesis, is recruited to chromatin in a ligand-independent manner and co-localized with ERM-NM-1 binding events. Furthermore, pertubation of AP-2M-NM-3 expression disrupts ERM-NM-1 DNA binding, long-range chromatin interactions, and gene transcription. Using ChIP-seq, we show that AP-2M-NM-3 and ERM-NM-1 binding occurs in close proximity on a genome-wide scale. The majority of these shared genomic regions are also occupied by the pioneer factor, FoxA1. AP-2M-NM-3 is required for efficient FoxA1 binding and vice versa. Finally, we show that most ERBS associated with long-range chromatin interactions are co-localized with both AP-2M-NM-3 and FoxA1. Together, our results suggest AP-2M-NM-3 is an essential factor in ERM-NM-1-mediated transcription, primarily working together with FoxA1 to facilitate ERM-NM-1 binding and long-range chromatin interactions. Genome-wide binding analysis of AP-2M-NM-3 and FoxA1 in MCF-7 with and without E2 (estradiol) stimulation using ChIP-Seq.
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Project description:Gene expression is controlled under spatial chromatin structures with short-range in topologically associating domains (TAD) and long-range chromatin interactions between TADs, compartments or chromosomes, and disruption of chromatin structure leads to human diseases. The mechanism of short-range chromatin interactions has been well characterized by loop-extrusion model, but little is known about how long-range chromatin interactions are organized. Here, we demonstrate that CTCF contributes to long-range chromatin interactions via phase separation. Surprisingly, RYBP is required for the phase separation and long-range chromatin organization of CTCF. Artificial CTCF phase seperation restores the long-range chromatin interactions and corresponding gene expression which were eliminated by RYBP depletion, and manipulation of CTCF phase separation also maintains pluripotency and inhibits differentation of embryonic stem cells. These findings support a model that long-range chromatin interactions are organized through phase sepearation of architectural protein, and further reveals the distinct mechanisms of architectural protein in organizing short-range and long-range chromatin interactions.
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Project description:Chromatin insulators organize the genome into distinct transcriptional domains and contribute to cell type-specific chromatin organization. However, factors regulating tissue-specific insulator function have not yet been discovered. Here we identify the RNA recognition motif-containing protein, Shep, as a direct interactor of two individual components of the gypsy insulator complex in Drosophila. Mutation of shep improves gypsy-dependent enhancer blocking, indicating a role as a negative regulator of insulator activity. Unlike ubiquitously expressed core gypsy insulator proteins, Shep is highly expressed in the central nervous system (CNS) with lower expression in other tissues. We developed a novel, quantitative tissue-specific barrier assay to demonstrate that Shep functions as a negative regulator of insulator activity in the CNS but not in muscle tissue. Additionally, mutation of shep alters insulator complex nuclear localization in the CNS but not other tissues. Consistent with negative regulatory activity, ChIP-seq analysis of Shep in a CNS-derived cell line indicates substantial genome-wide colocalization with a single gypsy insulator component but limited overlap with intact insulator complexes. Taken together, these data reveal a novel, tissue-specific mode of regulation of a chromatin insulator. ChIP-seq of Shep, Su(Hw), and Mod(mdg4)2.2 in Drosophila BG3 cells along with alternate antibodies
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Project description:Estrogen receptor α (ERα) is key player in the progression of breast cancer. ERα binds to DNA and mediates long-range chromatin interactions throughout the genome, but the underlying mechanism in this process is unclear. Here, we show that AP-2 motifs are highly enriched in the ERα binding sites (ERBS) identified from the recent ChIA-PET of ERα. More importantly, we demonstrate that AP-2γ (also known as TFAP2C), a member of the AP-2 family which has been implicated in breast cancer oncogenesis, is recruited to chromatin in a ligand-independent manner and co-localized with ERα binding events. Furthermore, pertubation of AP-2γ expression disrupts ERα DNA binding, long-range chromatin interactions, and gene transcription. Using ChIP-seq, we show that AP-2γ and ERα binding occurs in close proximity on a genome-wide scale. The majority of these shared genomic regions are also occupied by the pioneer factor, FoxA1. AP-2γ is required for efficient FoxA1 binding and vice versa. Finally, we show that most ERBS associated with long-range chromatin interactions are co-localized with both AP-2γ and FoxA1. Together, our results suggest AP-2γ is an essential factor in ERα-mediated transcription, primarily working together with FoxA1 to facilitate ERα binding and long-range chromatin interactions. Gene expression profiling of negative control (NC) and AP-2γ siRNA transfected MCF-7, with and without E2 (estradiol) stimulation using microarray.
2011-06-02 | E-GEOD-26740 | biostudies-arrayexpress
Project description:Estrogen receptor α (ERα) is key player in the progression of breast cancer. ERα binds to DNA and mediates long-range chromatin interactions throughout the genome, but the underlying mechanism in this process is unclear. Here, we show that AP-2 motifs are highly enriched in the ERα binding sites (ERBS) identified from the recent ChIA-PET of ERα. More importantly, we demonstrate that AP-2γ (also known as TFAP2C), a member of the AP-2 family which has been implicated in breast cancer oncogenesis, is recruited to chromatin in a ligand-independent manner and co-localized with ERα binding events. Furthermore, pertubation of AP-2γ expression disrupts ERα DNA binding, long-range chromatin interactions, and gene transcription. Using ChIP-seq, we show that AP-2γ and ERα binding occurs in close proximity on a genome-wide scale. The majority of these shared genomic regions are also occupied by the pioneer factor, FoxA1. AP-2γ is required for efficient FoxA1 binding and vice versa. Finally, we show that most ERBS associated with long-range chromatin interactions are co-localized with both AP-2γ and FoxA1. Together, our results suggest AP-2γ is an essential factor in ERα-mediated transcription, primarily working together with FoxA1 to facilitate ERα binding and long-range chromatin interactions.
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Project description:Chromatin insulators organize the genome into distinct transcriptional domains and contribute to cell type-specific chromatin organization. However, factors regulating tissue-specific insulator function have not yet been discovered. Here we identify the RNA recognition motif-containing protein, Shep, as a direct interactor of two individual components of the gypsy insulator complex in Drosophila. Mutation of shep improves gypsy-dependent enhancer blocking, indicating a role as a negative regulator of insulator activity. Unlike ubiquitously expressed core gypsy insulator proteins, Shep is highly expressed in the central nervous system (CNS) with lower expression in other tissues. We developed a novel, quantitative tissue-specific barrier assay to demonstrate that Shep functions as a negative regulator of insulator activity in the CNS but not in muscle tissue. Additionally, mutation of shep alters insulator complex nuclear localization in the CNS but not other tissues. Consistent with negative regulatory activity, ChIP-seq analysis of Shep in a CNS-derived cell line indicates substantial genome-wide colocalization with a single gypsy insulator component but limited overlap with intact insulator complexes. Taken together, these data reveal a novel, tissue-specific mode of regulation of a chromatin insulator.
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