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Total proteome analysis of DLD-1 cells expressing various degrons

ABSTRACT: Total Proteome analysis of various AID degron-bearing DLD-1 cells ( Nup96, Nup62, Nup188, TPR, Nup93, GANP, PCID2, Nup153, Nup160, Nup205) before and after addition of Auxin for 4-8 h.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell, Cell Culture

DISEASE(S): Colon Cancer

SUBMITTER: Alexei Arnaoutov

LAB HEAD: Mary Dasso

PROVIDER: PXD039407 | Pride | 2023-03-31

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	20200129_LFQ_set1_PEAKS_PTM_13_2.zip	Other
	20200129_LFQ_set2_PEAKS_PTM_13.zip	Other
	Description_of_columns_for_the_Results_spreadsheet.docx	Other
	LFQ1_peptides.xlsx	Xlsx
	LFQ1_proteins.xlsx	Xlsx

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Distinct Basket Nucleoporins roles in Nuclear Pore Function and Gene Expression

Project description:Nuclear pore complexes (NPCs) are important for cellular functions beyond nucleocytoplasmic trafficking, including genome organization and gene expression. This multi-faceted nature and the slow turnover of NPC components complicates investigations of how individual nucleoporins act in these diverse processes. To address this question, we used an Auxin-Induced Degron (AID) system to distinguish roles of basket nucleoporins Nup153, Nup50 and Tpr. Here, we provide MS data for the Nuclear Pore-enriched fraction of human DLD-1 cells, expressing CRISPR-engeneered degron, fused with the endogenous locus of corresponding basket NUPs, in the absence or presence of Auxin.

2020-06-30 | PXD020075 | Pride

Nup93 modulates spatiotemporal dynamics and function of the HOXA gene cluster during differentiation

Project description:The central role of nucleoporins is to transport RNA and proteins. In addtion, nucleoporins are also involved in gene regulation. Furthermore, nucleoporins - Nup93, Nup153, Nup98 and Nup210, directly associate with developmental genes and regulate developmental processes by direct association with developmental genes. Here, we identified genome wide binding profile of Nup93 - a core component of the nuclear pore complex in colorectal cancer cell line DLD-1 by ChIP-seq. Our ChIP-seq analysis revealed significant association of Nup93 with developmental genes and known enhancer marks such as H3K4me1 and H3K27Ac . We found that Nup93 shares binding sites with CTCF - the well known chromatin organizer, suggesting a functional overlap between Nup93 and CTCF in the organization and regulation of developmental gene expression such as the the HOXA gene cluster.

2021-12-06 | GSE130656 | GEO

Nucleoporin-mediated regulation of cell identity genes

Project description:The organization of the genome in the three-dimensional space of the nucleus is coupled with cell type-specific gene expression. However, how nuclear architecture influences transcription that governs cell identity remains unknown. Here, we show that Nuclear Pore Complex (NPC) components Nup93 and Nup153 bind super-enhancers (SE), regulatory structures that drive the expression of key genes that specify cell identity. We found that nucleoporin-associated SEs localize preferentially to the nuclear periphery, and absence of Nup153 and Nup93 results in dramatic transcriptional changes of SE-associated genes. Our results reveal a crucial role of NPC components in the regulation of cell type specifying genes and highlight nuclear architecture as a regulatory layer of genome functions in cell fate.

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Inherited folding programs: SILAC LC-MS of early G1 isolated nuclei formed in the presence or absence of Nup93- or RanGAP1-AID

Project description:Identity-specific interphase chromosome conformation must be re-established each time a cell divides. To understand how interphase folding is inherited, we developed an experimental approach that physically segregates mediators of G1 folding that are intrinsic to mitotic chromosomes from cytoplasmic factors. Proteins essential for nuclear transport, RanGAP1 and Nup93, were degraded in pro-metaphase arrested DLD-1 cells to prevent the establishment of nucleo-cytoplasmic transport during mitotic exit and isolate the decondensing mitotic chromatin of G1 daughter cells from the cytoplasm. Using this approach, we discover a transient folding intermediate entirely driven by chromosome-intrinsic factors. In addition to conventional compartmental segregation, this chromosome-intrinsic folding program leads to prominent genome-scale microcompartmentalization of mitotically bookmarked and cell type-specific cis-regulatory elements. The microcompartment conformation is formed during telophase and subsequently modulated by a second folding program driven by factors inherited through the cytoplasm in G1. This nuclear import-dependent folding program includes cohesin and factors involved in transcription and RNA processing. The combined and inter-dependent action of chromosome-intrinsic and cytoplasmic inherited folding programs determines the interphase chromatin conformation as cells exit mitosis. In our proteomics dataset we identify factors requiring nuclear import to access the genome at the end of mitosis.

2025-11-05 | PXD056346 | Pride

Nucleoporin Nup153 Regulates Stem Cell Pluripotency through Gene Silencing

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

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ChiP-chip profiling of Drosophila melanogaster cell lines to identify targets for nuclear pore proteins Nup153 and Megator.

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Novel function of NUP153 in HNF4α transcriptional upregulation contributes to promoting HBV replication

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

Nucleoporin-93 overexpression overcomes trafficking bottlenecks in metastasis of breast cancer

Project description:The integrative computational analysis we developed has assigned NUP93 with important roles in progression of mammary cancer, which we confirmed in animals. Surprisingly, NUP93 emerges from these studies as a master driver of metastasis. This conclusion was supported by functional characterization of two groups of naturally occurring mutant alleles. Remarkably, mammary cells overexpressing NUP93 display over-activation of multiple growth factor pathways, including the WNT/beta-catenin pathway. This route has previously been associated with colorectal tumors, but recent network-based analysis linked it to breast cancer (Koval and Katanaev, 2018). We conclude that NUP93 integrates and enhances not only WNT but also additional growth factor signals. Thus, by seizing an essential step common to multiple signaling routes, NUP93 acquires robust oncogenic attributes. Beyond the identification of augmented nuclear transport as a new hallmark of cancer, our study exposes tumor vulnerabilities and offers not only a new target for intervention but also a pharmacological strategy tailored to the subset of NUP93 overexpressors.

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Project description:Nup93 ChIP Seq

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The role of NUP93 in breast cancer

Project description:NUP93 expression inversely correlates with the survival of triple negative breast cancer patients. However, the role of NUP93 in tumor propagation has not yet been fully clarified. In this project we combined high-resolution imaging, migration assays and genetic analyses to demonstrate that NUP93 modulates actin cytoskeleton remodeling, epithelial-to-mesenchymal transition and invasion of triple negative breast cancer cells through direct interaction with the genome.

2020-01-18 | GSE137691 | GEO