Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA269747 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1699460.fastq.gz | Fastqsanger.gz | |||
| SRR1699451.fastq.gz | Fastqsanger.gz | |||
| SRR1699461.fastq.gz | Fastqsanger.gz | |||
| SRR1699452.fastq.gz | Fastqsanger.gz | |||
| SRR1699462.fastq.gz | Fastqsanger.gz |
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Project description:Nucleoporins (Nups) are a family of proteins best known as the constituent building blocks of nuclear pore complexes (NPCs), the transport channels that mediate nuclear transport. Recent evidence suggest that several Nups have additional roles in controlling the activation and silencing of developmental genes, however, the mechanistic details of these functions remain poorly understood. Here, we show that depletion of Nup153 in mouse embryonic stem cells (mESCs) causes the de-repression of developmental genes and induction of early differentiation. This loss of pluripotency is not associated with defects in global nucleo-cytoplasmic transport activity. Instead, Nup153 binds to the transcriptional start site (TSS) of developmental genes and mediates the recruitment of the polycomb repressive complex 1 (PRC1) to its target loci. Our results reveal a nuclear transport-independent role of Nup153 in maintaining stem cell pluripotency and introduce a role of NPC proteins in mammalian epigenetic gene silencing. RNA-seq, ChIP-Seq, and DamID-Seq for Nup153, Oct4, and key chromatin regulators in mouse ES cells and neural progenitors
2015-06-19 | E-GEOD-64008 | biostudies-arrayexpress
Project description:Nucleoporins (Nups) are a family of proteins best known as the constituent building blocks of nuclear pore complexes (NPCs), the transport channels that mediate nuclear transport. Recent evidence suggest that several Nups have additional roles in controlling the activation and silencing of developmental genes, however, the mechanistic details of these functions remain poorly understood. Here, we show that depletion of Nup153 in mouse embryonic stem cells (mESCs) causes the de-repression of developmental genes and induction of early differentiation. This loss of pluripotency is not associated with defects in global nucleo-cytoplasmic transport activity. Instead, Nup153 binds to the transcriptional start site (TSS) of developmental genes and mediates the recruitment of the polycomb repressive complex 1 (PRC1) to its target loci. Our results reveal a nuclear transport-independent role of Nup153 in maintaining stem cell pluripotency and introduce a role of NPC proteins in mammalian epigenetic gene silencing.
2015-06-19 | GSE64008 | GEO
Project description:We used RNA-seq approach to distinguish roles of basket nucleoporins Nup153, Nup50, and Tpr in transcription and nucleocytoplasmic trafficking. AID-mediated depletion of BSK-NUPs caused rapid and drastic changes in transcriptomic profiles within two hours of auxin addition. Changes upon Tpr nucleoporin loss were distinct from Nup153 and Nup50, but similar to changes upon loss of export factor NXF1 and GANP subunit of the TREX-2 mRNA export complex. Altogether, we demonstrated a unique role of Tpr nucleoporin in regulating genes expression through mRNA export.
2020-06-04 | GSE132363 | GEO
Project description:Reprogramming to pluripotency through a somatic stem cell intermediate
| PRJNA189293 | ENA
Project description:Cellular binary fate decisions require the progeny to silence genes associated with the alternative fate. The major subsets of alpha:beta T cells have been extensively studied as a model system for fate decisions. While the transcription factor RUNX3 is required for the initiation of Cd4 silencing in CD8 T cell progenitors, it is not required to maintain the silencing of Cd4 and other helper T lineage genes. The other runt domain containing protein, RUNX1, silences Cd4 in an earlier T cell progenitor, but this silencing is reversed whereas the gene silencing after RUNX3 expression is not reverse. Therefore, we hypothesized that RUNX3 and not RUNX1 recruits other factors that maintains the silencing of helper T lineage genes in CD8 T cells. To this end, we performed a proteomics screen of RUNX1 and RUNX3 to determine candidate silencing factors.
2019-11-12 | PXD007511 | Pride
Project description: Not available
| S-EPMC8784167 | biostudies-literature
Project description:Establishment of cell lineage specification, maintenance of cellular states and cellular responses to developmental cues rely on gene regulation and spatial genome organization during early development. Emerging data point to highly coordinated activity between epigenetic mechanisms that involve nuclear architecture, chromatin structure and chromatin organization. We show that the nuclear pore complex (NPC) basket protein, Nucleoporin 153 (NUP153) interacts with the nuclear architectural proteins, CTCF and cohesin, and mediates their binding across cis-regulatory elements in pluripotent mouse embryonic stem (ES) cells. NUP153 depletion results in altered occupancy of architectural proteins coupled with differential changes in transcription. This affect is most prevalent at the bivalent genes. To provide molecular insights onto NUP153-mediated gene regulation, we utilized Epidermal Growth Factor (EGF)-inducible immediate early gene (IEG) loci, which we identified as NUP153 targets. IEG transcription is regulated through a POL II pause-release mechanism. We provide evidence that NUP153 is critical for CTCF and cohesin occupancy and subsequent POL II recruitment to the IEG proximal-promoter sites during the paused state. In particular, establishment of a poised IEG chromatin environment relies on co-regulatory function of NUP153 and CTCF, which underlies efficient and timely IEG transcription at the NPC. Our results uncover a key role for the mammalian NPC in distribution of chromatin architectural proteins and demonstrate that NUP153 acts as a cis-acting factor that causally links the NPC to chromatin organization during transcription regulation.
2020-05-21 | GSE135646 | GEO
Project description:Establishment of cell lineage specification, maintenance of cellular states and cellular responses to developmental cues rely on gene regulation and spatial genome organization during early development. Emerging data point to highly coordinated activity between epigenetic mechanisms that involve nuclear architecture, chromatin structure and chromatin organization. We show that the nuclear pore complex (NPC) basket protein, Nucleoporin 153 (NUP153) interacts with the nuclear architectural proteins, CTCF and cohesin, and mediates their binding across cis-regulatory elements in pluripotent mouse embryonic stem (ES) cells. NUP153 depletion results in altered occupancy of architectural proteins coupled with differential changes in transcription. This affect is most prevalent at the bivalent genes. To provide molecular insights onto NUP153-mediated gene regulation, we utilized Epidermal Growth Factor (EGF)-inducible immediate early gene (IEG) loci, which we identified as NUP153 targets. IEG transcription is regulated through a POL II pause-release mechanism. We provide evidence that NUP153 is critical for CTCF and cohesin occupancy and subsequent POL II recruitment to the IEG proximal-promoter sites during the paused state. In particular, establishment of a poised IEG chromatin environment relies on co-regulatory function of NUP153 and CTCF, which underlies efficient and timely IEG transcription at the NPC. Our results uncover a key role for the mammalian NPC in distribution of chromatin architectural proteins and demonstrate that NUP153 acts as a cis-acting factor that causally links the NPC to chromatin organization during transcription regulation.
2020-05-21 | GSE135645 | GEO
Project description:Background & Aims: Nucleoporin 153 (NUP153) is known to facilitate the nuclear entry of the human immunodeficiency virus (HIV) nucleocapsid. Studies had also showed that immature hepatitis B virus (HBV) nucleocapsids can be arrested by NUP153, allowing them to further mature. In this study, we investigated the impact and specific mechanisms of NUP153 on HBV replication. Methods: NUP153 was knocked down using RNA interference or over-expressed through an expression plasmid in HBV cell models or in vivo in HBV-replicating mice. Luciferase reporter assays were employed to assess the activities of viral or host factor promoters. Cytoplasmic and nuclear fractionation experiments were conducted to analyze the subcellular distribution of proteins and HBV RNA. Results: In the present study, we found that HBV induced significant upregulation of NUP153 mRNA and protein in HBV cell models and HBV infected patients. Overexpression of NUP153 would markedly increase covalently closed circular DNA (cccDNA) transcription activity and progeny virus production, while downregulation of NUP153 could significantly inhibit HBV replication without affecting HBV cccDNA level directly. Similar results were observed in mice model hydrodynamically injected (HDI) with 1.2×HBV plasmid. HBV promoter assays revealed that NUP153 could promote HBV core promoter activity, likely in a hepatocyte nuclear factor 4α (HNF4α) dependent manner. Mechanistically, ERK signaling was required for NUP153-mediated promotion of HNF4α and HBV replication. Conclusions: The study here suggested that host factor NUP153 which reciprocally upregulated by the virus, is an important positive regulator of HBV replication. It also suggested that the NUP153-HBV positive feedback loop could serve as a potential therapeutic target.
2025-09-20 | GSE276333 | GEO
Project description:To understand the mechanisms through which JunB regulates Tregs-mediated immune regulation, we examined the global gene expression profiles in the JunB WT and KO Tregs by performing RNA sequencing (RNA-seq) analysis.
2019-05-07 | GSE129060 | GEO