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Genome occupancy of NIPBL in mouse P19 teratocarcinoma cells.

ABSTRACT: Genome occupancy of NIPBL in mouse P19 teratocarcinoma cells.

PROVIDER: PRJNA548964 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9305140.fastq.gz	Fastqsanger.gz
	SRR9305139.fastq.gz	Fastqsanger.gz

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Genome occupancy of NIPBL in mouse P19 teratocarcinoma cells.

2020-01-01 | GSE132784 | GEO

Transcriptome analysis upon Nipbl, Brd2 and Brd4 knockdown in P19 cells

Project description:Mutations in NIPBL are the major cause of Cornelia de Lange Syndrome (CdLS). NIPBL is the cohesin loading factor and has recently been associated with the BET (Bromodomains and Extra Terminal (ET) domain) proteins BRD2 and BRD4. Related to this, a CdLS-like phenotype has been described associated to BRD4 mutations. To understand the relationship between NIPBL and BET proteins, we have performed RNA-Seq expression analysis following depletion of the different proteins in mouse P19 teratocarcinoma cells. Results indicate that genes regulated by NIPBL largely overlap with those regulated by BRD4 but not with those regulated by BRD2.

2020-01-01 | GSE132785 | GEO

Transcriptome analysis upon Nipbl, Brd2 and Brd4 knockdown in P19 cells

Project description:Transcriptome analysis upon Nipbl, Brd2 and Brd4 knockdown in P19 cells

| PRJNA548966 | ENA

Calcium Signaling Prompts NIPBL Recruitment at Active Enhancers and Promoters via Distinct Mechanisms to Reconstruct Genome Compartmentalization

Project description:During developmental progression the genomes of immune cells undergo large-scale changes in chromatin folding. However, insights into the signals and epigenetics that induce alterations in nuclear architecture remain rudimentary. Here, we found that calcium influx rapidly recruited the cohesin-loading factor NIPBL to thousands of binding sites to dictate widespread changes in compartment segregation. The induction of NIPBL-binding was coordinate with increased P300, BRG1 and RNA Polymerase II co-occupancy, via different kinetics at active enhancers and promoters. Through acute degradation system, we found that enhancers, rather than promoters, are dependent on BAF complexes to induce NIPBL recruitment. Finally, we found that calcium signaling acts universally to orchestrate rapid redistribution of NIPBL in both primary innate and adaptive immune cells. Collectively, these data reveal how calcium signaling regulates NIPBL occupancy to orchestrate nuclear architecture.

2020-10-10 | GSE154051 | GEO

Transcription factors form a ternary complex with NIPBL/MAU2 to localize cohesin at enhancers

Project description:While the cohesin complex is a key player in genome architecture, how it localizes to specific chromatin sites is not well understood. Recently, we and others have proposed that direct interactions with transcription factors (TFs) lead to the localization of the cohesin-loader complex (NIPBL/MAU2) within enhancers. Here, we identify two clusters of protein-protein interaction (PPI) motifs within the NIPBL sequence that regulate NIPBL dynamics, interactome, and NIPBL-dependent transcriptional programs. These PPIMs directly interact with chromatin-associated proteins, including TFs and one of them is necessary for the maintenance of the NIPBL-MAU2 heterodimer. Finally, using the glucocorticoid receptor (GR) as a model, we investigate its interaction surfaces with NIPBL and MAU2 using AlphaFold2 and surface plasmon resonance to uncover a TF-NIPBL-MAU2 ternary complex and present its importance in GR-dependent gene regulation.

2025-04-17 | PXD058574 | Pride

Gene expression in F9 teratocarcinoma cells

Project description:Dr. Esko's laboratory focuses on the structure, function, and biosynthesis of glycoproteins and proteoglycans. This laboratory also works on the design and synthesis of small molecule inhibitors of glycosylation. Gene expression in F9 teratocarcinoma cells: Study of the differential expression of glycosyltransferases, sulfotransferases and proteoglycan core proteins in F9 teratocarcinoma cells before and after differentiation with retinoic acid/theophylline/cAMP. Published data indicated that differentiation of the cells induces the synthesis of anticoagulant heparin-like compounds and a large increase in overall glycosaminoglycan synthesis.

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p19-WT and p19-T111BpyAla treatment of extracted small RNAs

Project description:small RNA fractions were treated with either p19-WT or T111BpyAla to evaluate the catalytic ability of p19-T111BpyAla compared to the WT protein in degrading miRNAs

2023-04-28 | GSE229272 | GEO

Pioneer factors orchestrate tissue-specific cohesin-NIPBL chromatin entry and 3D genome organization

Project description:Cohesin complex shapes 3D genome organization by extruding DNA loops, yet the mechanisms underlying its chromatin entry remain poorly understood. Here, we reveal that the cohesin loader NIPBL exhibits highly tissue-specific chromatin binding, in stark contrast to the conserved binding profiles of CTCF and RAD21. We identify pioneer transcription factors (TFs), notably FOXA1, as key mediators of NIPBL recruitment to chromatin. FOXA1 directs NIPBL to intra-TAD regions, enabling symmetric loop extrusion, while factors like ETS1 target NIPBL to TAD boundaries, supporting one-sided extrusion. Rapid depletion of FOXA1 disrupts NIPBL binding and intra-TAD loops, whereas loss of NIPBL impairs both intra-TAD and inter-TAD interactions, highlighting their roles in 3D genome folding. Strikingly, a recurrent FOXA1 mutation (R219S) in prostate cancer redirects NIPBL to TAD boundaries by recognizing a non-canonical motif, fostering a more insulated and tumor-aggressive genome. Evolutionary analysis points to a potential conserved role for TF-NIPBL cooperation in cohesin chromatin entry across species with tissue-specific adaptations. Our findings reveal that pioneer factors orchestrate cohesin loading to shape tissue-specific chromatin accessibility and 3D genome dynamics, a mechanism hijacked in diseases like cancer to rewire gene expression.

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Distribution of chromatin features in mouse P19 embryonal carcinoma cells

Project description:CHIP to investigate Hmgn2 binding in P19 undifferentiated and differentiated neuronal cells.

2018-08-03 | GSE118031 | GEO

Decreasing Wapl dosage partially corrects transcriptome phenotypes in Nipbl-/+ embryonic mouse brain

Project description:Cohesin rings interact with DNA and modulate expression of thousands of genes. NIPBL loads cohesin onto chromosomes and WAPL takes it off. Heterozygous mutations in NIPBL lead to a developmental disorder called Cornelia de Lange syndrome. Nipbl heterozygous mice are a good model for this disease. Mutations in WAPL were not known to cause disease or gene expression changes in mammals. Here we show dysregulation of >1000 genes in Wapl-/+embryonic mouse brains. The patterns of dysregulation are highly similar in Wapl and Nipbl heterozygotes, suggesting that Wapl mutations may cause disease in humans. Since WAPL and NIPBL have opposite effects on cohesin’s association with DNA, we asked whether a heterozygous Wapl mutation could correct phenotypes seen in Nipbl heterozygous mice. In fact, both gene expression and embryonic growth are partially corrected. Our data are consistent with the view that cohesin dynamics play a key role in regulating gene expression.

2022-10-11 | GSE203014 | GEO

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